Cytokines in RA
Cytokines in rheumatoid arthritis
During the disease process, the role of the lymphocytes expands. Different cells respond upon stimulation by cytokines and a complex process of cell interactions, angiogenesis and bone destruction begins.
The lining of the synovium contains synoviocytes of type A and B. Type A shows similarity with macrophages. Synoviocyte B cells release the cytokines interleukin-8 (IL-8), IL-6, prostaglandins and metalloproteinases. IL-8 attracts lymphocytes in the capillaries in order to invade the sublining of the synovium. The metalloproteinases and prostaglandins are responsible for the destruction of cartilage and bone. The macrophages in the inflammatory tissue produce important mediators for all other cells involved.
Tumor necrosis factor-α (TNF-α) and IL-1 released by the macrophages are involved in bone destruction, stimulate type B synoviocytes to release their products and enhance lymphocyte invasion. The accumulation of specific CD4+ T lymphocytes occurs in the sub-lining of the synovial tissues. The macrophages also release IL-12 and IL-18, which stimulate the T lymphocytes. Upon this stimulation, the cells release interferon γ (IFN-γ), which in turn stimulates the macrophages.
Besides the inflammation, angiogenesis is an important process in rheumatoid arthritis. The newly formed capillaries provide oxygen and nutrients for the hypertrophic synovium and allow many lymphocytes to invade the tissue.
Inflammatory cytokines include all of the following EXCEPT