Функциональные нарушения макрофагов при ревматоидном артрите и атеросклерозе

Одна из актуальных и развивающихся проблем современной медицинской науки – поражение сердечно-сосудистой системы, обусловленное атеросклеротическим поражением сосудов, у больных с иммуновоспалительными ревматическими заболеваниями (РЗ). Ревматоидный артрит (РА) – заболевание с известно высоким кардиоваскулярным риском. Установлено, что основная причина высокой преждевременной смертности при РА связана с сердечно-сосудистыми осложнениями, обусловленными ускоренным прогрессированием атеросклероза. Распространенность субклинических и клинических проявлений атеросклероза при РА составляет 35–59%. Наиболее часто ССО развиваются у больных РА с низким или умеренным кардиоваскулярным риском, но с высокой клинико-иммунологической активностью болезни. Привлекает внимание схожесть механизмов иммунопатогенеза классических РЗ и хронического low-grade воспаления при атеросклерозе. По современным представлениям, хроническое воспаление, развитие которого связывают с неконтролируемой активацией как врожденного, так и приобретенного иммунитета, играет фундаментальную роль на всех стадиях аутоиммунных РЗ и атеросклеротического процесса. Среди многочисленных «иммунных» клеток и медиаторов, участвующих в иммунопатогенезе как РА, так и атеросклероза, важное место занимают моноциты-макрофаги и цитокины, продуцируемые ими. Дисбаланс между M1- и M2-фенотипами макрофагов рассматривается в качестве одной из причин развития РА. Определена важная роль М1-макрофагов, продуцирующих два основных «провоспалительных» цитокина – интерлейкин 6 (ИЛ6) и ИЛ23, – в поддержании ревматоидного воспаления. Проводятся поиски возможных механизмов возникновения дизрегуляции М1/М2-макрофагов при воспалении. Изучение ключевого патогенетического фактора в развитии аутоиммунного и атеросклеротического воспаления – активированных моноцитов-макрофагов – не только углубит знания о патогенезе хронического воспаления, но и позволит расширить представления о патогенетическом и предиктивном значении «клеточных» маркеров и перевести на качественно новый уровень раннюю диагностику атеросклеротического поражения при РА.

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