![]() ![]() The inflammatory infiltrate in RA includes T cells, B cells and dendritic cells, and in approximately 20% of patients lymphoid neogenesis develops with the formation of ectopic germinal centres. Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease, characterised by inflammatory polyarthritis and joint damage resulting in progressive disability. Moreover, the significant increase in the peripheral blood pre-switch memory B cells in patients who underwent specific TNF-blockade with infliximab indicates that trafficking of memory B cells into inflamed tissue in RA patients is regulated by TNF and can be corrected by neutralising TNF. The data suggest that decreases in peripheral blood IgD +CD27 + pre-switch memory B cells in RA reflect their accumulation in the synovial tissue. Finally, anti-TNF therapy increased the frequency of pre-switch IgD +CD27 memory B cells in the peripheral blood. Notably, both pre-switch IgD +CD27 + and post-switch IgD -CD27 + memory B cells accumulate in the synovial membrane of RA patients. ![]() RA patients, independent of disease duration, have a significantly lower frequency of peripheral blood pre-switch IgD +CD27 + memory B cells than healthy individuals, whereas post-switch IgD -CD27 + accumulate with increased disease duration. Additionally, the possible role of TNF in causing disturbances in memory B cell subsets in RA patients was assessed in a clinical trial with the specific TNF-neutralising antibody, infliximab. The frequency and distribution of B cell subsets in the peripheral blood and synovial membrane of active RA patients with long-standing disease have been analysed. Additionally, the possible role of tumour necrosis factor (TNF) in regulating changes in specific peripheral blood memory B cell subsets in RA is still unclear. Disturbances in peripheral blood memory B cell subpopulations have been observed in various autoimmune diseases, but have not been fully delineated in rheumatoid arthritis (RA). ![]()
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