Abstract
The paper summarizes the data available in the literature and those from the authors' studies on the molecular and cellular mechanisms of apoptosis and their state in rheumatoid arthritis (RA). Impaired apoptotic processes in RA are one of the causes of synovial cell hyperactivation that leads to the increased inflammatory process, synovial hyperplasia, and progression of the disease as a whole. The most important feature of a cellular continuum in the affected synovial fluid is the coexistence of just two mechanisms that control apoptosis: 1) a traditional activation mechanism leading to progressive joint inflammation and destruction and 2) an inhibitory mechanism implemented through the expression of proapoptotic molecules. The apoptotic factors are a useful tool for assessing the prognosis of RA and a promising target for pharmacotherapy.
Highlights
Apoptosis as a factor for organizing autoimmune inflammation in rheumatoid arthritis Dubikov A.I.1, Kalinichenko S.G.2, Matveeva N.Yu
Impaired apoptotic processes in RA are one of the causes of synovial cell hyperactivation that leads to the increased inflammatory process, synovial hyperplasia, and progression of the disease as a whole
The most important feature of a cellular continuum in the affected synovial fluid is the coexistence of just two mechanisms that control apoptosis: 1) a traditional activation mechanism leading to progressive joint inflammation and destruction and 2) an inhibitory mechanism implemented through the expression of proapoptotic molecules
Summary
Apoptosis as a factor for organizing autoimmune inflammation in rheumatoid arthritis Dubikov A.I.1, Kalinichenko S.G.2, Matveeva N.Yu.2. 2. Апоптотические синовиоциты и молекулярные факторы апоптоза в синовиальной оболочке коленного сустава при РА: а – TUNEL-иммунореактивные ядра (стрелки) в периваскулярном инфильтрате на ранней стадии РА; б – массивный апоптоз фибробластоподобных клеток в стромальном слое синовии на поздней стадии РА (стрелки); в – bcl-2- Выявленная тенденция позволяет оценивать состояние апоптоза в клетках синовиальной оболочки у больных РА по уровню экспрессии этих факторов в клетках костного мозга.
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