mimmunМедицинская иммунологияMedical Immunology (Russia)1563-06252313-741XSPb RAACI10.15789/1563-0625-PVO-2386mimmun-2386Research ArticleОБЗОРЫREVIEWSПатогенетическое значение клеточного инфильтрата при иммуновоспалительных ревматических заболеванияхPathogenetic value of cell infiltrate in immunoinflammatory rheumatic diseaseshttps://orcid.org/0000-0001-6246-4482СаидовМ. З.SaidovM. Z.

Саидов Марат Зиявдинович - доктор медицинских наук, профессор, заведующий кафедрой патологической физиологии/

367000, Республика Дагестан, г. Махачкала, пл. Ленина, 1. Тел.: 8 (988) 300-90-45

Saidov Marat Z. - PhD, MD (Medicine), Professor, Head, Department of Pathological Physiology.

Makhachkala

marat.saidov.55@mail.ruФГБОУ ВО Дагестанский государственный медицинский университетРоссияDagestan State Medical UniversityRussian Federation20212012202123612391270Copyright © Саидов М.З., 20212021Саидов М.З.Saidov M.Z.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.mimmun.ru/mimmun/article/view/2386

Клеточный инфильтрат является морфологическим субстратом иммуновоспалительных ревматических заболеваний. Cистемная прогрессирующая дезорганизация рыхлой волокнистой соединительной ткани сопровождается утратой толерантности с собственными аутоантигенами, активацией клеток макрофагально-моноцитарного ряда и аутореактивных клонов Т- и В-лимфоцитов. Гиперпродукция провоспалительных хемо- и цитокинов, локальные адгезионные лиганд-рецепторные взаимодействия, эндотелиальная реакция и ангиогенез способствуют формированию клеточного инфильтрата, эктопических лимфоидных структур и ГЗТ-гранулем in situ. Аутоиммунный ответ является следствием последовательных системных и местных молекулярно-клеточных событий, в которых задействованы механизмы врожденного и адаптивного иммунитета. При интерпретации иммунопатогенеза ревматических заболеваний применяются все модели и схемы, принятые в области фундаментальной иммунологии. Это модель МНС-рестрикции, модель молекулярной мимикрии, или перекрестной (кросс) АГ-презентации, модель срыва центральной или периферической толерантности к ауто-АГ, модель кандидатных «триггеров» аутоиммунных и аутовоспалительных процессов, модель ассоциаций аллелей МНС I и II классов с конкретными, нозологически уникальными, ревматическими заболеваниями.

Cell infiltrate is a morphological substrate of immunoinflammatory rheumatic diseases. The systemic wide progressive disorganization of loose fibrous connective tissue is accompanied by the loss of tolerance with its own autoantigenes, activation of macrophagal-monocyte cells and autoreactive clones of T and B lymphocytes. Hyperproduction of pro-inflammatory chemokines and cytokines, local adhesive ligandreceptor interactions, endothelial reaction and angiogenesis contribute to the formation of cell infiltrate, ectopic lymphoid structures and GZT-granulomas in situ. The autoimmune response is the result of successive systemic and local molecular cellular events in which the mechanisms of congenital and adaptive immunity are involved. When interpreting immunopathogenesis of rheumatic diseases, all models and schemes adopted in the field of fundamental immunology are used. This is a model of MHC-restrictions, a model of molecular mimicry, or cross of the antigen presentation, a model of disrupting central or peripheral tolerance to auto-antigens, a model of candidate “triggers” of autoimmune and autoinflammatory processes, a model of associations of alleles MHC I and II classes with specific, nosologically unique, rheumatic diseases.

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The authors declare that there are no conflicts of interest present.