Apoptosis as a factor for organizing autoimmune inflammation in rheumatoid arthritis

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.

Keywords

• chronic rheumatic diseases
• mechanisms of apoptosis
• p53
• bcl-2
• mdm2
• puma
• caspases
• pharmacotherapy