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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">nnp</journal-id><journal-title-group><journal-title xml:lang="en">Neurology, Neuropsychiatry, Psychosomatics</journal-title><trans-title-group xml:lang="ru"><trans-title>Неврология, нейропсихиатрия, психосоматика</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2074-2711</issn><issn pub-type="epub">2310-1342</issn><publisher><publisher-name>"IMA-Press", LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/2074-2711-2026-1-4-13</article-id><article-id custom-type="elpub" pub-id-type="custom">nnp-2769</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>LECTURES</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ЛЕКЦИЯ</subject></subj-group></article-categories><title-group><article-title>The role of microglia in the pathogenesis of multiple sclerosis</article-title><trans-title-group xml:lang="ru"><trans-title>Роль микроглии в патогенезе рассеянного склероза</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6647-0572</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Карчевская</surname><given-names>А. Е</given-names></name><name name-style="western" xml:lang="en"><surname>Karchevskaya</surname><given-names>A. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Анна Евгеньевна Карчевская</p><p>117485; ул. Бутлерова, 5А; 119048; ул. Трубецкая, 8, стр. 2; Москва</p></bio><bio xml:lang="en"><p>Anna Yevgenyevna Karchevskaya</p><p>117485; 5A, Butlerova St.; 119991; 8, Trubetskaya St., Build. 2; Moscow</p></bio><email xlink:type="simple">anna.karchevsky@ihna.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8039-9194</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Набиев</surname><given-names>Ш. Р.</given-names></name><name name-style="western" xml:lang="en"><surname>Nabiev</surname><given-names>Sh. R.</given-names></name></name-alternatives><bio xml:lang="ru"><p>119048; ул. Трубецкая, 8, стр. 2; Москва</p></bio><bio xml:lang="en"><p>119991; 8, Trubetskaya St., Build. 2; Moscow</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3831-414X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Оганесян</surname><given-names>И. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Oganesyan</surname><given-names>I. Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>119048; ул. Трубецкая, 8, стр. 2; Москва</p></bio><bio xml:lang="en"><p>119991; 8, Trubetskaya St., Build. 2; Moscow</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7330-633X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Воскресенcкая</surname><given-names>О. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Voskresenskaya</surname><given-names>O. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>119048; ул. Трубецкая, 8, стр. 2; Москва</p></bio><bio xml:lang="en"><p>119991; 8, Trubetskaya St., Build. 2; Moscow</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБУН «Институт высшей нервной деятельности и нейрофизиологии РАН»; ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» (Сеченовский Университет)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences; I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia (Sechenov University)</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» (Сеченовский Университет)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia (Sechenov University)</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>22</day><month>02</month><year>2026</year></pub-date><volume>18</volume><issue>1</issue><fpage>4</fpage><lpage>13</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Karchevskaya A.E., Nabiev S.R., Oganesyan I.Y., Voskresenskaya O.N., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Карчевская А.Е., Набиев Ш.Р., Оганесян И.Ю., Воскресенcкая О.Н.</copyright-holder><copyright-holder xml:lang="en">Karchevskaya A.E., Nabiev S.R., Oganesyan I.Y., Voskresenskaya O.N.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://nnp.ima-press.net/nnp/article/view/2769">https://nnp.ima-press.net/nnp/article/view/2769</self-uri><abstract><p>   Microglia are currently considered to be the main representatives of myeloid cells in the central nervous system (CNS) and perform a number of homeostatic functions. In response to damaging effects and changes in the CNS, microglia are activated and can perform both neuroinflammatory and neuroprotective roles. A number of studies indicate that chronic activation of microglia contributes to the development of demyelinating diseases. This review examines the contribution of microglia to the development and progression of multiple sclerosis, analyses its involvement in the demyelination process, and discusses potential therapeutic approaches aimed at modulating its activity.</p></abstract><trans-abstract xml:lang="ru"><p>   Микроглия в настоящее время считается главным представителем миелоидных клеток в центральной нервной системе (ЦНС) и выполняет ряд гомеостатических функций. В ответ на повреждающие воздействия и изменения в ЦНС микроглия активируется и может выполнять как нейровоспалительную, так и нейропротективную роль. Ряд исследований указывают на то, что хроническая активация микроглии способствует развитию демиелинизирующих заболеваний. В данном обзоре рассматривается вклад микроглии в развитие и прогрессирование рассеянного склероза, анализируются ее участие в процессе демиелинизации и потенциальные терапевтические подходы, направленные на модуляцию ее активности.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>рассеянный склероз</kwd><kwd>микроглия</kwd><kwd>патогенез</kwd><kwd>нейровоспаление</kwd><kwd>биомаркеры</kwd><kwd>цереброспинальная жидкость</kwd></kwd-group><kwd-group xml:lang="en"><kwd>multiple sclerosis</kwd><kwd>microglia</kwd><kwd>pathogenesis</kwd><kwd>neuroinflammation</kwd><kwd>biomarkers</kwd><kwd>cerebrospinal fluid</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование не имело спонсорской поддержки</funding-statement><funding-statement xml:lang="en">The investigation has not been sponsored</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Jia Y, Zhang D, Li H, et al. Activation of FXR by ganoderic acid A promotes remyelination in multiple sclerosis via anti-inflammation and regeneration mechanism. Biochem Pharmacol. 2021;185:114422. doi: 10.1016/j.bcp.2021.114422</mixed-citation><mixed-citation xml:lang="en">Jia Y, Zhang D, Li H, et al. Activation of FXR by ganoderic acid A promotes remyelination in multiple sclerosis via anti-inflammation and regeneration mechanism. Biochem Pharmacol. 2021;185:114422. doi: 10.1016/j.bcp.2021.114422</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Wingerchuk DM, Carter JL. Multiple sclerosis: current and emerging disease-modifying therapies and treatment strategies. Mayo Clin Proc. 2014 Feb;89(2):225-40. doi: 10.1016/j.mayocp.2013.11.002</mixed-citation><mixed-citation xml:lang="en">Wingerchuk DM, Carter JL. Multiple sclerosis: current and emerging disease-modifying therapies and treatment strategies. Mayo Clin Proc. 2014 Feb;89(2):225-40. doi: 10.1016/j.mayocp.2013.11.002</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Мельников МВ, Свиридова АА, Роговский ВС и др. Роль макрофагов в развитии нейровоспаления при рассеянном склерозе. Журнал неврологии и психиатрии им. С.С. Корсакова. 2022;122(5):51-6. doi: 10.17116/jnevro202212205151</mixed-citation><mixed-citation xml:lang="en">Melnikov MV, Sviridova AA, Rogovskii VS, Boyko AN, Pashenkov MV. The role of macrophages in the development of neuroinflammation in multiple sclerosis. S.S. Korsakov Journal of Neurology and Psychiatry. 2022;122(5):51-6 (In Russ.). doi: 10.17116/jnevro202212205151</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Prineas JW, Lee S. Microglia subtypes in acute, subacute, and chronic multiple sclerosis. J Neuropathol Exp Neurol. 2023;82(8):674-94. doi: 10.1093/jnen/nlad046</mixed-citation><mixed-citation xml:lang="en">Prineas JW, Lee S. Microglia subtypes in acute, subacute, and chronic multiple sclerosis. J Neuropathol Exp Neurol. 2023;82(8):674-94. doi: 10.1093/jnen/nlad046</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Prineas JW, Parratt JD. Multiple sclerosis: microglia, monocytes, and macrophage-mediated demyelination. J Neuropathol Exp Neurol. 2021;80(10):975-96. doi: 10.1093/jnen/nlab083</mixed-citation><mixed-citation xml:lang="en">Prineas JW, Parratt JD. Multiple sclerosis: microglia, monocytes, and macrophage-mediated demyelination. J Neuropathol Exp Neurol. 2021;80(10):975-96. doi: 10.1093/jnen/nlab083</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Kuhlmann T, Moccia M, Coetzee T, et al. Multiple sclerosis progression: time for a new mechanism-driven framework. Lancet Neurol. 2023;22(1):78-88. doi: 10.1016/S1474-4422(22)00289-7</mixed-citation><mixed-citation xml:lang="en">Kuhlmann T, Moccia M, Coetzee T, et al. Multiple sclerosis progression: time for a new mechanism-driven framework. Lancet Neurol. 2023;22(1):78-88. doi: 10.1016/S1474-4422(22)00289-7</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Dobson R, Giovannoni G. Multiple sclerosis – a review. Eur J Neurol. 2019;26(1):27-40. doi: 10.1111/ene.13819</mixed-citation><mixed-citation xml:lang="en">Dobson R, Giovannoni G. Multiple sclerosis – a review. Eur J Neurol. 2019;26(1):27-40. doi: 10.1111/ene.13819</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Voet S, Prinz M, van Loo G. Microglia in central nervous system inflammation and multiple sclerosis pathology. Trends Mol Med. 2019;25(2):112-23. doi: 10.1016/j.molmed.2018.11.005</mixed-citation><mixed-citation xml:lang="en">Voet S, Prinz M, van Loo G. Microglia in central nervous system inflammation and multiple sclerosis pathology. Trends Mol Med. 2019;25(2):112-23. doi: 10.1016/j.molmed.2018.11.005</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">El Mahdaoui S, Husted SR, Hansen MB, et al. Cerebrospinal fluid soluble CD27 is associated with CD8+ T cells, B cells and biomarkers of B cell activity in relapsing-remitting multiple sclerosis. J Neuroimmunol. 2023;381:578128. doi: 10.1016/j.jneuroim.2023.578128</mixed-citation><mixed-citation xml:lang="en">El Mahdaoui S, Husted SR, Hansen MB, et al. Cerebrospinal fluid soluble CD27 is associated with CD8+ T cells, B cells and biomarkers of B cell activity in relapsing-remitting multiple sclerosis. J Neuroimmunol. 2023;381:578128. doi: 10.1016/j.jneuroim.2023.578128</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Sloane E, Ledeboer A, Seibert W, et al. Anti-inflammatory cytokine gene therapy decreases sensory and motor dysfunction in experimental Multiple Sclerosis: MOG-EAE behavioral and anatomical symptom treatment with cytokine gene therapy. Brain Behav Immun. 2009;23(1):92-100. doi: 10.1016/j.bbi.2008.09.004</mixed-citation><mixed-citation xml:lang="en">Sloane E, Ledeboer A, Seibert W, et al. Anti-inflammatory cytokine gene therapy decreases sensory and motor dysfunction in experimental Multiple Sclerosis: MOG-EAE behavioral and anatomical symptom treatment with cytokine gene therapy. Brain Behav Immun. 2009;23(1):92-100. doi: 10.1016/j.bbi.2008.09.004</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Maroto-Garcia J, Martinez-Escribano A, Delgado-Gil V, et al. Biochemical biomarkers for multiple sclerosis. Clin Chim Acta. 2023;117471. doi: 10.1016/j.cca.2023.1174711</mixed-citation><mixed-citation xml:lang="en">Maroto-Garcia J, Martinez-Escribano A, Delgado-Gil V, et al. Biochemical biomarkers for multiple sclerosis. Clin Chim Acta. 2023;117471. doi: 10.1016/j.cca.2023.1174711</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Guerrero BL, Sicotte NL. Microglia in Multiple Sclerosis: Friend or Foe? Front Immunol. 2020;11:374. doi: 10.3389/fimmu.2020.00374</mixed-citation><mixed-citation xml:lang="en">Guerrero BL, Sicotte NL. Microglia in Multiple Sclerosis: Friend or Foe? Front Immunol. 2020;11:374. doi: 10.3389/fimmu.2020.00374</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Walsh AD, Nguyen LT, Binder MD. miRNAs in microglia: important players in multiple sclerosis pathology. ASN Neuro. 2021;13:1759091420981182. doi: 10.1177/1759091420981182</mixed-citation><mixed-citation xml:lang="en">Walsh AD, Nguyen LT, Binder MD. miRNAs in microglia: important players in multiple sclerosis pathology. ASN Neuro. 2021;13:1759091420981182. doi: 10.1177/1759091420981182</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Yong VW. Microglia in multiple sclerosis: Protectors turn destroyers. Neuron. 2022;110(21):3534-48. doi: 10.1016/j.neuron.2022.06.023</mixed-citation><mixed-citation xml:lang="en">Yong VW. Microglia in multiple sclerosis: Protectors turn destroyers. Neuron. 2022;110(21):3534-48. doi: 10.1016/j.neuron.2022.06.023</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Sen MK, Mahns DA, Coorssen JR, Shortland PJ. The roles of microglia and astrocytes in phagocytosis and myelination: Insights from the cuprizone model of multiple sclerosis. Glia. 2022;70(7):1215-50. doi: 10.1002/glia.24148</mixed-citation><mixed-citation xml:lang="en">Sen MK, Mahns DA, Coorssen JR, Shortland PJ. The roles of microglia and astrocytes in phagocytosis and myelination: Insights from the cuprizone model of multiple sclerosis. Glia. 2022;70(7):1215-50. doi: 10.1002/glia.24148</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Talebi F, Ghorbani S, Chan WF, et al. MicroRNA-142 regulates inflammation and T cell differentiation in an animal model of multiple sclerosis. J Neuroinflammation. 2017;14:1-14. doi: 10.1186/s12974-017-0832-7</mixed-citation><mixed-citation xml:lang="en">Talebi F, Ghorbani S, Chan WF, et al. MicroRNA-142 regulates inflammation and T cell differentiation in an animal model of multiple sclerosis. J Neuroinflammation. 2017;14:1-14. doi: 10.1186/s12974-017-0832-7</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Chaudhuri AD, Yelamanchili SV, Marcondes MCG, Fox HS. Up-regulation of microRNA-142 in simian immunodeficiency virus encephalitis leads to repression of sirtuin1. FASEB J. 2013;27(9):3720. doi: 10.1096/fj.13-232678</mixed-citation><mixed-citation xml:lang="en">Chaudhuri AD, Yelamanchili SV, Marcondes MCG, Fox HS. Up-regulation of microRNA-142 in simian immunodeficiency virus encephalitis leads to repression of sirtuin1. FASEB J. 2013;27(9):3720. doi: 10.1096/fj.13-232678</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Kessler W, Thomas C, Kuhlmann T. Microglia activation in periplaque white matter in multiple sclerosis depends on age and lesion type, but does not correlate with oligoden-droglial loss. Acta Neuropathologica. 2023;146(6):817-28. doi: 10.1007/s00401-023-02645-2</mixed-citation><mixed-citation xml:lang="en">Kessler W, Thomas C, Kuhlmann T. Microglia activation in periplaque white matter in multiple sclerosis depends on age and lesion type, but does not correlate with oligoden-droglial loss. Acta Neuropathologica. 2023;146(6):817-28. doi: 10.1007/s00401-023-02645-2</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Michailidou I, Willems JG, Kooi E, et al. Complement C 1q-C 3-associated synaptic changes in multiple sclerosis hippocampus. Ann Neurol. 2015;77(6): 1007-26. doi: 10.1002/ana.24398</mixed-citation><mixed-citation xml:lang="en">Michailidou I, Willems JG, Kooi E, et al. Complement C 1q-C 3-associated synaptic changes in multiple sclerosis hippocampus. Ann Neurol. 2015;77(6): 1007-26. doi: 10.1002/ana.24398</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Sherafat A, Pfeiffer F, Reiss AM, et al. Microglial neuropilin-1 promotes oligodendrocyte expansion during development and remyelination by trans-activating platelet-derived growth factor receptor. Nature Communicat. 2021;12(1):2265. doi: 10.1038/s41467-021-22532-2</mixed-citation><mixed-citation xml:lang="en">Sherafat A, Pfeiffer F, Reiss AM, et al. Microglial neuropilin-1 promotes oligodendrocyte expansion during development and remyelination by trans-activating platelet-derived growth factor receptor. Nature Communicat. 2021;12(1):2265. doi: 10.1038/s41467-021-22532-2</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Van Wageningen TA, Vlaar E, Kooij G, et al. Regulation of microglial TMEM119 and P2RY12 immunoreactivity in multiple sclerosis white and grey matter lesions is dependent on their inflammatory environment. Acta Neuropathol Commun. 2019;7:1-16. doi: 10.1186/s40478-019-0850-z</mixed-citation><mixed-citation xml:lang="en">Van Wageningen TA, Vlaar E, Kooij G, et al. Regulation of microglial TMEM119 and P2RY12 immunoreactivity in multiple sclerosis white and grey matter lesions is dependent on their inflammatory environment. Acta Neuropathol Commun. 2019;7:1-16. doi: 10.1186/s40478-019-0850-z</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Nuesslein-Hildesheim B, Ferrero E, Schmid C, et al. Remibrutinib (LOU064) inhibits neuroinflammation driven by B cells and myeloid cells in preclinical models of multiple sclerosis. J Neuroinflammation. 2023;20(1):194. doi: 10.1186/s12974-023-02877-9</mixed-citation><mixed-citation xml:lang="en">Nuesslein-Hildesheim B, Ferrero E, Schmid C, et al. Remibrutinib (LOU064) inhibits neuroinflammation driven by B cells and myeloid cells in preclinical models of multiple sclerosis. J Neuroinflammation. 2023;20(1):194. doi: 10.1186/s12974-023-02877-9</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Cignarella F, Filipello F, Bollman B, et al. TREM2 activation on microglia promotes myelin debris clearance and remyelination in a model of multiple sclerosis. Acta Neuropathologica. 2020;140:513-34. doi: 10.1007/s00401-020-02193-z</mixed-citation><mixed-citation xml:lang="en">Cignarella F, Filipello F, Bollman B, et al. TREM2 activation on microglia promotes myelin debris clearance and remyelination in a model of multiple sclerosis. Acta Neuropathologica. 2020;140:513-34. doi: 10.1007/s00401-020-02193-z</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Masuda T, Sankowski R, Staszewski O, et al. Spatial and temporal heterogeneity of mouse and human microglia at single-cell resolution. Nature. 2019;566(7744):388-92. doi: 10.1038/s41586-019-0924-x</mixed-citation><mixed-citation xml:lang="en">Masuda T, Sankowski R, Staszewski O, et al. Spatial and temporal heterogeneity of mouse and human microglia at single-cell resolution. Nature. 2019;566(7744):388-92. doi: 10.1038/s41586-019-0924-x</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Fiedler T, Fairless R, Pichi K, et al. Co-modulation of TNFR1 and TNFR2 in an animal model of multiple sclerosis. J Neuroinflammation. 2023;20(1):100. doi: 10.1186/s12974-023-02784-z</mixed-citation><mixed-citation xml:lang="en">Fiedler T, Fairless R, Pichi K, et al. Co-modulation of TNFR1 and TNFR2 in an animal model of multiple sclerosis. J Neuroinflammation. 2023;20(1):100. doi: 10.1186/s12974-023-02784-z</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Pegoretti V, Bauer J, Fischer R, et al. Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS. J Neuroinflammation. 2023;20(1):106. doi: 10.1186/s12974-023-02785-y</mixed-citation><mixed-citation xml:lang="en">Pegoretti V, Bauer J, Fischer R, et al. Sequential treatment with a TNFR2 agonist and a TNFR1 antagonist improves outcomes in a humanized mouse model for MS. J Neuroinflammation. 2023;20(1):106. doi: 10.1186/s12974-023-02785-y</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Tsouki F, Williams A. Multifaceted involvement of microglia in gray matter pathology in multiple sclerosis. Stem Cells. 2021;39(8):993-1007. doi: 10.1002/stem.3374</mixed-citation><mixed-citation xml:lang="en">Tsouki F, Williams A. Multifaceted involvement of microglia in gray matter pathology in multiple sclerosis. Stem Cells. 2021;39(8):993-1007. doi: 10.1002/stem.3374</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Zrzavy T, Hametner S, Wimmer I, et al. Loss of “homeostatic” microglia and patterns of their activation in active multiple sclerosis. Brain. 2017;140(7):1900-13. doi: 10.1093/brain/awx113</mixed-citation><mixed-citation xml:lang="en">Zrzavy T, Hametner S, Wimmer I, et al. Loss of “homeostatic” microglia and patterns of their activation in active multiple sclerosis. Brain. 2017;140(7):1900-13. doi: 10.1093/brain/awx113</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Gomez Morillas A, Besson VC, Lerouet D. Microglia and neuroinflammation: what place for P2RY12? Int J Mol Sci. 2021;22(4):1636. doi: 10.3390/ijms22041636</mixed-citation><mixed-citation xml:lang="en">Gomez Morillas A, Besson VC, Lerouet D. Microglia and neuroinflammation: what place for P2RY12? Int J Mol Sci. 2021;22(4):1636. doi: 10.3390/ijms22041636</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Mercurio D, Fumagalli S, Schafer MK, et al. Protein expression of the microglial marker Tmem119 decreases in association with morphological changes and location in a mouse model of traumatic brain injury. Front Cell Neurosci. 2022;16:820127. doi: 10.3389/fncel.2022.820127</mixed-citation><mixed-citation xml:lang="en">Mercurio D, Fumagalli S, Schafer MK, et al. Protein expression of the microglial marker Tmem119 decreases in association with morphological changes and location in a mouse model of traumatic brain injury. Front Cell Neurosci. 2022;16:820127. doi: 10.3389/fncel.2022.820127</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Gruchot J, Weyers V, Göttle P, et al. The molecular basis for remyelination failure in multiple sclerosis. Cells. 2019;8(8):825. doi: 10.3390/cells8080825</mixed-citation><mixed-citation xml:lang="en">Gruchot J, Weyers V, Göttle P, et al. The molecular basis for remyelination failure in multiple sclerosis. Cells. 2019;8(8):825. doi: 10.3390/cells8080825</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Ton AMM, Vasconcelos CCF, Alvarenga RMP. Benign multiple sclerosis: aspects of cognition and neuroimaging. Arquivos de Neuro-Psiquiatria. 2017;75(6):394-401. doi: 10.1590/0004-282x20170043</mixed-citation><mixed-citation xml:lang="en">Ton AMM, Vasconcelos CCF, Alvarenga RMP. Benign multiple sclerosis: aspects of cognition and neuroimaging. Arquivos de Neuro-Psiquiatria. 2017;75(6):394-401. doi: 10.1590/0004-282x20170043</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Капканец ДВ, Белов СЕ, Долгушин МБ, Бойко АН. Признак парамагнитного обода при рассеянном склерозе. Неврология, нейропсихиатрия, психосоматика. 2023;15(4):94-9. doi: 10.14412/2074-2711-2023-4-94-99</mixed-citation><mixed-citation xml:lang="en">Kapkanets DV, Belov SE, Dolgushin MB, Boyko AN. Paramagnetic rim sign in multiple sclerosis. Nevrologiya, neiropsikhiatriya, psikhosomatika = Neurology, Neuropsychiatry, Psychosomatics. 2023;15(4):94-9 (In Russ.). doi: 10.14412/2074-2711-2023-4-94-99</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Garcia-Hernandez R, Cerdan Cerda A, Trouve Carpena A, et al. Mapping microglia and astrocyte activation in vivo using diffusion MRI. Sci Adv. 2022;8(21):eabq2923. doi: 10.1126/sciadv.abq2923</mixed-citation><mixed-citation xml:lang="en">Garcia-Hernandez R, Cerdan Cerda A, Trouve Carpena A, et al. Mapping microglia and astrocyte activation in vivo using diffusion MRI. Sci Adv. 2022;8(21):eabq2923. doi: 10.1126/sciadv.abq2923</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Chataway J, Williams T, Li V, et al. Clinical trials for progressive multiple sclerosis: progress, new lessons learned, and remaining challenges. Lancet Neurol. 2024;23(3):277-301. doi: 10.1016/S1474-4422(24)00027-9</mixed-citation><mixed-citation xml:lang="en">Chataway J, Williams T, Li V, et al. Clinical trials for progressive multiple sclerosis: progress, new lessons learned, and remaining challenges. Lancet Neurol. 2024;23(3):277-301. doi: 10.1016/S1474-4422(24)00027-9</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Abourbeh G, Theze B, Maroy R, et al. Imaging microglial/macrophage activation in spinal cords of experimental autoimmune encephalomyelitis rats by positron emission tomography using the mitochondrial 18 kDa translocator protein radioligand [18F]DPA-714. J Neurosci. 2012;32(17):5728-36. doi: 10.1523/JNEUROSCI.2900-11.2012</mixed-citation><mixed-citation xml:lang="en">Abourbeh G, Theze B, Maroy R, et al. Imaging microglial/macrophage activation in spinal cords of experimental autoimmune encephalomyelitis rats by positron emission tomography using the mitochondrial 18 kDa translocator protein radioligand [18F]DPA-714. J Neurosci. 2012;32(17):5728-36. doi: 10.1523/JNEUROSCI.2900-11.2012</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Hamzaoui M, Garcia J, Boffa G, et al. Positron Emission Tomography with [(18) F]-DPA-714 Unveils a Smoldering Component in Most Multiple Sclerosis Lesions which Drives Disease Progression. Ann Neurol. 2023;94(2):366-83. doi: 10.1002/ana.26657</mixed-citation><mixed-citation xml:lang="en">Hamzaoui M, Garcia J, Boffa G, et al. Positron Emission Tomography with [(18) F]-DPA-714 Unveils a Smoldering Component in Most Multiple Sclerosis Lesions which Drives Disease Progression. Ann Neurol. 2023;94(2):366-83. doi: 10.1002/ana.26657</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Van der Weijden CWJ, Meilof JF, van der Hoorn A, et al. The Future of PET Imaging in Multiple Sclerosis: Characterisation of Individual White Matter Lesions. J Clin Med. 2025;14(13). doi: 10.3390/jcm14134439</mixed-citation><mixed-citation xml:lang="en">Van der Weijden CWJ, Meilof JF, van der Hoorn A, et al. The Future of PET Imaging in Multiple Sclerosis: Characterisation of Individual White Matter Lesions. J Clin Med. 2025;14(13). doi: 10.3390/jcm14134439</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Cantoni C, Bollman B, Licastro D, et al. TREM2 regulates microglial cell activation in response to demyelination in vivo. Acta Neuropathologica. 2015;129:429-47. doi: 10.1007/s00401-015-1388-1</mixed-citation><mixed-citation xml:lang="en">Cantoni C, Bollman B, Licastro D, et al. TREM2 regulates microglial cell activation in response to demyelination in vivo. Acta Neuropathologica. 2015;129:429-47. doi: 10.1007/s00401-015-1388-1</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Zetterberg H. Fluid biomarkers for microglial activation and axonal injury in multiple sclerosis. Acta Neurol Scand. 2017;136:15-7. doi: 10.1111/ane.12845</mixed-citation><mixed-citation xml:lang="en">Zetterberg H. Fluid biomarkers for microglial activation and axonal injury in multiple sclerosis. Acta Neurol Scand. 2017;136:15-7. doi: 10.1111/ane.12845</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Öhrfelt A, Axelsson M, Malmeström C, et al. Soluble TREM-2 in cerebrospinal fluid from patients with multiple sclerosis treated with natalizumab or mitoxantrone. Mult Scler. 2016 Oct;22(12):1587-95. doi: 10.1177/1352458515624558</mixed-citation><mixed-citation xml:lang="en">Öhrfelt A, Axelsson M, Malmeström C, et al. Soluble TREM-2 in cerebrospinal fluid from patients with multiple sclerosis treated with natalizumab or mitoxantrone. Mult Scler. 2016 Oct;22(12):1587-95. doi: 10.1177/1352458515624558</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">Ioannides ZA, Csurhes PA, Swayne A, et al. Correlations between macrophage/microglial activation marker sTREM-2 and measures of T-cell activation, neuroaxonal damage and disease severity in multiple sclerosis. Mult Scler J Exp Transl Clin. 2021 Jun 3;7(2):20552173211019772. doi: 10.1177/20552173211019772</mixed-citation><mixed-citation xml:lang="en">Ioannides ZA, Csurhes PA, Swayne A, et al. Correlations between macrophage/microglial activation marker sTREM-2 and measures of T-cell activation, neuroaxonal damage and disease severity in multiple sclerosis. Mult Scler J Exp Transl Clin. 2021 Jun 3;7(2):20552173211019772. doi: 10.1177/20552173211019772</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">Rival M, Galoppin M, Thouvenot E. Biological markers in early multiple sclerosis: the paved way for radiologically isolated syndrome. Front Immunol. 2022;13:866092. doi: 10.3389/fimmu.2022.866092</mixed-citation><mixed-citation xml:lang="en">Rival M, Galoppin M, Thouvenot E. Biological markers in early multiple sclerosis: the paved way for radiologically isolated syndrome. Front Immunol. 2022;13:866092. doi: 10.3389/fimmu.2022.866092</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">Beliёn J, Swinnen S, D’hondt R, et al. CHIT1 at diagnosis predicts faster disability progression and reflects early microglial activation in multiple sclerosis. Nat Commun. 2024;15(1):5013. doi: 10.1038/s41467-024-49312-y</mixed-citation><mixed-citation xml:lang="en">Beliёn J, Swinnen S, D’hondt R, et al. CHIT1 at diagnosis predicts faster disability progression and reflects early microglial activation in multiple sclerosis. Nat Commun. 2024;15(1):5013. doi: 10.1038/s41467-024-49312-y</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Vankriekelsvenne E, Chrzanowski U, Manzhula K, et al. Transmembrane protein 119 is neither a specific nor a reliable marker for microglia. Glia. 2022;70(6):1170-90. doi: 10.1002/glia.24164</mixed-citation><mixed-citation xml:lang="en">Vankriekelsvenne E, Chrzanowski U, Manzhula K, et al. Transmembrane protein 119 is neither a specific nor a reliable marker for microglia. Glia. 2022;70(6):1170-90. doi: 10.1002/glia.24164</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">Reich DS, Arnold DL, Vermersch P, et al. Safety and efficacy of tolebrutinib, an oral brain-penetrant BTK inhibitor, in relapsing multiple sclerosis: a phase 2b, randomised, double-blind, placebo-controlled trial. Lancet Neurol. 2021;20(9):729-38. doi: 10.1016/s1474-4422(21)00237-4</mixed-citation><mixed-citation xml:lang="en">Reich DS, Arnold DL, Vermersch P, et al. Safety and efficacy of tolebrutinib, an oral brain-penetrant BTK inhibitor, in relapsing multiple sclerosis: a phase 2b, randomised, double-blind, placebo-controlled trial. Lancet Neurol. 2021;20(9):729-38. doi: 10.1016/s1474-4422(21)00237-4</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Martin E, Aigrot MS, Grenningloh R, et al. Brutonуs tyrosine kinase inhibition promotes myelin repair. Brain Plasticity. 2019;5(2):123-33. doi: 10.3233/bpl-200100</mixed-citation><mixed-citation xml:lang="en">Martin E, Aigrot MS, Grenningloh R, et al. Brutonуs tyrosine kinase inhibition promotes myelin repair. Brain Plasticity. 2019;5(2):123-33. doi: 10.3233/bpl-200100</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Gruber R, Blazier A, Lee L, et al. Evaluating the effect of btk inhibitor tolebrutinib in human tri-culture (P1-1. Virtual). Neurology. 2022;98(18_supplement):2594. doi: 10.1212/WNL.98.18_supplement.2594</mixed-citation><mixed-citation xml:lang="en">Gruber R, Blazier A, Lee L, et al. Evaluating the effect of btk inhibitor tolebrutinib in human tri-culture (P1-1. Virtual). Neurology. 2022;98(18_supplement):2594. doi: 10.1212/WNL.98.18_supplement.2594</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Krämer J, Bar-Or A, Turner TJ, Wiendl H. Bruton tyrosine kinase inhibitors for multiple sclerosis. Nat Rev Neurol. 2023;19(5):289-304. doi: 10.1038/s41582-023-00800-7</mixed-citation><mixed-citation xml:lang="en">Krämer J, Bar-Or A, Turner TJ, Wiendl H. Bruton tyrosine kinase inhibitors for multiple sclerosis. Nat Rev Neurol. 2023;19(5):289-304. doi: 10.1038/s41582-023-00800-7</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Langlois J, Lange S, Ebeling M, et al. Fenebrutinib, a Brutonуs tyrosine kinase inhibitor, blocks distinct human microglial signaling pathways. J Neuroinflammation. 2024;21(1):276. doi: 10.1186/s12974-024-03267-5</mixed-citation><mixed-citation xml:lang="en">Langlois J, Lange S, Ebeling M, et al. Fenebrutinib, a Brutonуs tyrosine kinase inhibitor, blocks distinct human microglial signaling pathways. J Neuroinflammation. 2024;21(1):276. doi: 10.1186/s12974-024-03267-5</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Bar-Or A, Dufek M, Budincevic H, et al. Safety and efficacy of fenebrutinib in relapsing multiple sclerosis (FENopta): a multicentre, double-blind, randomised, placebo-controlled, phase 2 trial and open-label extension study. Lancet Neurol. 2025;24(8):656-66. doi: 10.1016/s1474-4422(25)00174-7</mixed-citation><mixed-citation xml:lang="en">Bar-Or A, Dufek M, Budincevic H, et al. Safety and efficacy of fenebrutinib in relapsing multiple sclerosis (FENopta): a multicentre, double-blind, randomised, placebo-controlled, phase 2 trial and open-label extension study. Lancet Neurol. 2025;24(8):656-66. doi: 10.1016/s1474-4422(25)00174-7</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Fox RJ, Bar-Or A, Traboulsee A, et al; HERCULES Trial Group. Tolebrutinib in Nonrelapsing Secondary Progressive Multiple Sclerosis. N Engl J Med. 2025 May 15;392(19):1883-92. doi: 10.1056/NEJMoa2415988</mixed-citation><mixed-citation xml:lang="en">Fox RJ, Bar-Or A, Traboulsee A, et al; HERCULES Trial Group. Tolebrutinib in Nonrelapsing Secondary Progressive Multiple Sclerosis. N Engl J Med. 2025 May 15;392(19):1883-92. doi: 10.1056/NEJMoa2415988</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Montalban X, Vermersch P, Arnold DL, et al. Safety and efficacy of evobrutinib in relapsing multiple sclerosis (evolutionRMS1 and evolutionRMS2): two multicentre, randomised, double-blind, active-controlled, phase 3 trials. Lancet Neurol. 2024;23(11):1119-32. doi: 10.1016/s1474-4422(24)00328-4</mixed-citation><mixed-citation xml:lang="en">Montalban X, Vermersch P, Arnold DL, et al. Safety and efficacy of evobrutinib in relapsing multiple sclerosis (evolutionRMS1 and evolutionRMS2): two multicentre, randomised, double-blind, active-controlled, phase 3 trials. Lancet Neurol. 2024;23(11):1119-32. doi: 10.1016/s1474-4422(24)00328-4</mixed-citation></citation-alternatives></ref><ref id="cit54"><label>54</label><citation-alternatives><mixed-citation xml:lang="ru">Gruchot J, Lein F, Lewen I, et al. Siponimod modulates the reaction of microglial cells to pro-inflammatory stimulation. Int J Mol Sci. 2022;23(21):13278. doi: 10.3390/ijms232113278</mixed-citation><mixed-citation xml:lang="en">Gruchot J, Lein F, Lewen I, et al. Siponimod modulates the reaction of microglial cells to pro-inflammatory stimulation. Int J Mol Sci. 2022;23(21):13278. doi: 10.3390/ijms232113278</mixed-citation></citation-alternatives></ref><ref id="cit55"><label>55</label><citation-alternatives><mixed-citation xml:lang="ru">O’Sullivan C, Schubart A, Mir AK, Dev KK. The dual S1PR1/S1PR5 drug BAF312 (Siponimod) attenuates demyelination in organotypic slice cultures. J Neuroinflammation. 2016;13:1-14. doi: 10.1186/s12974-016-0494-x</mixed-citation><mixed-citation xml:lang="en">O’Sullivan C, Schubart A, Mir AK, Dev KK. The dual S1PR1/S1PR5 drug BAF312 (Siponimod) attenuates demyelination in organotypic slice cultures. J Neuroinflammation. 2016;13:1-14. doi: 10.1186/s12974-016-0494-x</mixed-citation></citation-alternatives></ref><ref id="cit56"><label>56</label><citation-alternatives><mixed-citation xml:lang="ru">Noda H, Takeuchi H, Mizuno T, Suzumura A. Fingolimod phosphate promotes the neuroprotective effects of microglia. J Neuroimmunol. 2013;256(1-2):13-8. doi: 10.1016/j.jneuroim.2012.12.005</mixed-citation><mixed-citation xml:lang="en">Noda H, Takeuchi H, Mizuno T, Suzumura A. Fingolimod phosphate promotes the neuroprotective effects of microglia. J Neuroimmunol. 2013;256(1-2):13-8. doi: 10.1016/j.jneuroim.2012.12.005</mixed-citation></citation-alternatives></ref><ref id="cit57"><label>57</label><citation-alternatives><mixed-citation xml:lang="ru">Dietrich M, Hecker C, Martin E, et al. Increased Remyelination and Proregenerative Microglia Under Siponimod Therapy in Mechanistic Models. Neurol Neuroimmunol Neuroinflammat. 2022;9(3):e1161. doi: 10.1212/NXI.0000000000001161</mixed-citation><mixed-citation xml:lang="en">Dietrich M, Hecker C, Martin E, et al. Increased Remyelination and Proregenerative Microglia Under Siponimod Therapy in Mechanistic Models. Neurol Neuroimmunol Neuroinflammat. 2022;9(3):e1161. doi: 10.1212/NXI.0000000000001161</mixed-citation></citation-alternatives></ref><ref id="cit58"><label>58</label><citation-alternatives><mixed-citation xml:lang="ru">Jorgensen LO, Hyrlov K, Elkjaer M, et al. Cladribine modifies functional properties of microglia. Clin Exp Immunol. 2020;201(3):328-40. doi: 10.1111/cei.13473</mixed-citation><mixed-citation xml:lang="en">Jorgensen LO, Hyrlov K, Elkjaer M, et al. Cladribine modifies functional properties of microglia. Clin Exp Immunol. 2020;201(3):328-40. doi: 10.1111/cei.13473</mixed-citation></citation-alternatives></ref><ref id="cit59"><label>59</label><citation-alternatives><mixed-citation xml:lang="ru">Aybar F, Perez MJ, Marcora MS, et al. 2-Chlorodeoxyadenosine (Cladribine) preferentially inhibits the biological activity of microglial cells. Int Immunopharmacol. 2022;105: 108571. doi: 10.1016/j.intimp.2022.108571</mixed-citation><mixed-citation xml:lang="en">Aybar F, Perez MJ, Marcora MS, et al. 2-Chlorodeoxyadenosine (Cladribine) preferentially inhibits the biological activity of microglial cells. Int Immunopharmacol. 2022;105: 108571. doi: 10.1016/j.intimp.2022.108571</mixed-citation></citation-alternatives></ref><ref id="cit60"><label>60</label><citation-alternatives><mixed-citation xml:lang="ru">Singh V, Voss EV, Benardais K, Stangel M. Effects of 2-chlorodeoxyadenosine (Cladribine) on primary rat microglia. J Neuroimmun Pharmacol. 2012;7:939-50. doi: 10.1007/s11481-012-9387-7</mixed-citation><mixed-citation xml:lang="en">Singh V, Voss EV, Benardais K, Stangel M. Effects of 2-chlorodeoxyadenosine (Cladribine) on primary rat microglia. J Neuroimmun Pharmacol. 2012;7:939-50. doi: 10.1007/s11481-012-9387-7</mixed-citation></citation-alternatives></ref><ref id="cit61"><label>61</label><citation-alternatives><mixed-citation xml:lang="ru">Бахтиярова КЗ, Бойко АН, Власов ЯВ и др. Рекомендации по использованию кладрибина в таблетках для патогенетического лечения пациентов с высокоактивным рассеянным склерозом. Неврология, нейропсихиатрия, психосоматика. 2020;12(3):93-9. doi: 10.14412/2074-2711-2020-3-93-99</mixed-citation><mixed-citation xml:lang="en">Bakhtiyarova KZ, Boyko AN, Vlasov YaV, et al. Recommendations for the use of cladribine tablets for the pathogenetic treatment of patients with highly active multiple sclerosis. Nevrologiya, neiropsikhiatriya, psikhosomatika = Neurology, Neuropsychiatry, Psychosomatics. 2020;12(3):93-9 (In Russ.). doi: 10.14412/2074-2711-2020-3-93-99</mixed-citation></citation-alternatives></ref><ref id="cit62"><label>62</label><citation-alternatives><mixed-citation xml:lang="ru">Boyko AN, Boyko OV. Cladribine tabletsу potential role as a key example of selective immune reconstitution therapy in multiple sclerosis. Degener Neurol Neuromuscul Dis. 2018 May 3;8:35-44. doi: 10.2147/DNND.S161450</mixed-citation><mixed-citation xml:lang="en">Boyko AN, Boyko OV. Cladribine tabletsу potential role as a key example of selective immune reconstitution therapy in multiple sclerosis. Degener Neurol Neuromuscul Dis. 2018 May 3;8:35-44. doi: 10.2147/DNND.S161450</mixed-citation></citation-alternatives></ref><ref id="cit63"><label>63</label><citation-alternatives><mixed-citation xml:lang="ru">Giovannoni G, Boyko A, Correale J, et al. A plain language summary on assessing the long-term effectiveness of cladribine tablets in people living with relapsing multiple sclerosis: The CLASSIC-MS study. Neurodegener Dis Manag. 2023;13(5):261-8. doi: 10.2217/nmt-2023-0018</mixed-citation><mixed-citation xml:lang="en">Giovannoni G, Boyko A, Correale J, et al. A plain language summary on assessing the long-term effectiveness of cladribine tablets in people living with relapsing multiple sclerosis: The CLASSIC-MS study. Neurodegener Dis Manag. 2023;13(5):261-8. doi: 10.2217/nmt-2023-0018</mixed-citation></citation-alternatives></ref><ref id="cit64"><label>64</label><citation-alternatives><mixed-citation xml:lang="ru">Giovannoni G, Boyko A, Correale J, et al. Long-term follow-up of patients with a first clinical demyelinating event (clinically isolated syndrome) who received cladribine tablets in CLASSIC-MS: Findings for the ORACLE-MS cohort. Mult Scler. 2025;31(1):44-58. doi: 10.1177/13524585241302170</mixed-citation><mixed-citation xml:lang="en">Giovannoni G, Boyko A, Correale J, et al. Long-term follow-up of patients with a first clinical demyelinating event (clinically isolated syndrome) who received cladribine tablets in CLASSIC-MS: Findings for the ORACLE-MS cohort. Mult Scler. 2025;31(1):44-58. doi: 10.1177/13524585241302170</mixed-citation></citation-alternatives></ref><ref id="cit65"><label>65</label><citation-alternatives><mixed-citation xml:lang="ru">Tastan B, Arioz BI, Tufekci KU, et al. Dimethyl fumarate alleviates NLRP3 inflammasome activation in microglia and sickness behavior in LPS-challenged mice. Front Immunol. 2021;12:737065. doi: 10.3389/fimmu.2021.737065</mixed-citation><mixed-citation xml:lang="en">Tastan B, Arioz BI, Tufekci KU, et al. Dimethyl fumarate alleviates NLRP3 inflammasome activation in microglia and sickness behavior in LPS-challenged mice. Front Immunol. 2021;12:737065. doi: 10.3389/fimmu.2021.737065</mixed-citation></citation-alternatives></ref><ref id="cit66"><label>66</label><citation-alternatives><mixed-citation xml:lang="ru">Rosito M, Testi C, Parisi G, et al. Exploring the use of dimethyl fumarate as microglia modulator for neurodegenerative diseases treatment. Antioxidants. 2020;9(8):700. doi: 10.3390/antiox9080700</mixed-citation><mixed-citation xml:lang="en">Rosito M, Testi C, Parisi G, et al. Exploring the use of dimethyl fumarate as microglia modulator for neurodegenerative diseases treatment. Antioxidants. 2020;9(8):700. doi: 10.3390/antiox9080700</mixed-citation></citation-alternatives></ref><ref id="cit67"><label>67</label><citation-alternatives><mixed-citation xml:lang="ru">Мельников МВ, Шаранова СН, Коновалова ОЕ и др. Влияние глатирамера ацетата на функционирование Th1- и Th17-клеток у больных рассеянным склерозом. Журнал неврологии и психиатрии им. С.С. Корсакова. 2018;8(2):151-8. doi: 10.17116/jnevro2018118082121</mixed-citation><mixed-citation xml:lang="en">Melnikov MV, Sharanova SN, Konovalova OE, et al. The effect of glatiramer acetate on the functioning of Th1 and Th17 cells in patients with multiple sclerosis. S.S. Korsakov Journal of Neurology and Psychiatry. 2018;8(2):151-8 (In Russ.). doi: 10.17116/jnevro2018118082121</mixed-citation></citation-alternatives></ref><ref id="cit68"><label>68</label><citation-alternatives><mixed-citation xml:lang="ru">Sellebjerg F, Cadavid D, Steiner D, et al. Exploring potential mechanisms of action of natalizumab in secondary progressive multiple sclerosis. Ther Adv Neurol Disord. 2016;9(1):31-43. doi: 10.1177/1756285615615257</mixed-citation><mixed-citation xml:lang="en">Sellebjerg F, Cadavid D, Steiner D, et al. Exploring potential mechanisms of action of natalizumab in secondary progressive multiple sclerosis. Ther Adv Neurol Disord. 2016;9(1):31-43. doi: 10.1177/1756285615615257</mixed-citation></citation-alternatives></ref><ref id="cit69"><label>69</label><citation-alternatives><mixed-citation xml:lang="ru">Mindur JE, Ito N, Dhib-Jalbut S, Ito K. Early treatment with anti-VLA-4 mAb can prevent the infiltration and/or development of pathogenic CD11b&lt;sup&gt;+&lt;/sup&gt; CD4&lt;sup&gt;+&lt;/sup&gt; T cells in the CNS during progressive EAE. PloS One. 2014;9(6):e99068. doi: 10.1371/journal.pone.0099068</mixed-citation><mixed-citation xml:lang="en">Mindur JE, Ito N, Dhib-Jalbut S, Ito K. Early treatment with anti-VLA-4 mAb can prevent the infiltration and/or development of pathogenic CD11b&lt;sup&gt;+&lt;/sup&gt; CD4&lt;sup&gt;+&lt;/sup&gt; T cells in the CNS during progressive EAE. PloS One. 2014;9(6):e99068. doi: 10.1371/journal.pone.0099068</mixed-citation></citation-alternatives></ref><ref id="cit70"><label>70</label><citation-alternatives><mixed-citation xml:lang="ru">De Kleijn KMA, Martens GJM. Molecular Effects of FDA-Approved Multiple Sclerosis Drugs on Glial Cells and Neurons of the Central Nervous System. Int J Mol Sci. 2020;21(12):4229. doi: 10.3390/ijms21124229</mixed-citation><mixed-citation xml:lang="en">De Kleijn KMA, Martens GJM. Molecular Effects of FDA-Approved Multiple Sclerosis Drugs on Glial Cells and Neurons of the Central Nervous System. Int J Mol Sci. 2020;21(12):4229. doi: 10.3390/ijms21124229</mixed-citation></citation-alternatives></ref><ref id="cit71"><label>71</label><citation-alternatives><mixed-citation xml:lang="ru">Pul R, Moharregh-Khiabani D, Skuljec J, et al. Glatiramer acetate modulates TNF-α and IL-10 secretion in microglia and promotes their phagocytic activity. J Neuroimmun Pharmacol. 2011;6:381-8. doi: 10.1007/s11481-010-9248-1</mixed-citation><mixed-citation xml:lang="en">Pul R, Moharregh-Khiabani D, Skuljec J, et al. Glatiramer acetate modulates TNF-α and IL-10 secretion in microglia and promotes their phagocytic activity. J Neuroimmun Pharmacol. 2011;6:381-8. doi: 10.1007/s11481-010-9248-1</mixed-citation></citation-alternatives></ref><ref id="cit72"><label>72</label><citation-alternatives><mixed-citation xml:lang="ru">Ten Bosch GJ, Bolk J, Фt Hart BA, Laman JD. Multiple sclerosis is linked to MAPKERK overactivity in microglia. J Mol Med. 2021;99(8):1033-42. doi: 10.1007/s00109-021-02080-4</mixed-citation><mixed-citation xml:lang="en">Ten Bosch GJ, Bolk J, Фt Hart BA, Laman JD. Multiple sclerosis is linked to MAPKERK overactivity in microglia. J Mol Med. 2021;99(8):1033-42. doi: 10.1007/s00109-021-02080-4</mixed-citation></citation-alternatives></ref><ref id="cit73"><label>73</label><citation-alternatives><mixed-citation xml:lang="ru">Konen FF, Möhn N, Witte T, et al. Treatment of autoimmunity: the impact of disease-modifying therapies in multiple sclerosis and comorbid autoimmune disorders. Autoimmun Rev. 2023;22(5):103312. doi: 10.1016/j.autrev.2023.103312</mixed-citation><mixed-citation xml:lang="en">Konen FF, Möhn N, Witte T, et al. Treatment of autoimmunity: the impact of disease-modifying therapies in multiple sclerosis and comorbid autoimmune disorders. Autoimmun Rev. 2023;22(5):103312. doi: 10.1016/j.autrev.2023.103312</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
