Abstract
Abstract Clinical benefits from anti-TNF and B cell depletion therapy in the treatment of rheumatoid arthritis (RA) highlight the important roles of both TNF-α and B cells in the pathogenesis of RA. However, the precise role of B cells in pathogenesis of RA is not yet defined. Human TNF-α transgenic mice (hTNFtg) develop a chronic inflammatory-erosive joint disease similar to RA, and provide a useful model for studying disease pathogenesis. During progression of the disease in the knee of hTNFtg mice, the adjacent popliteal lymph node (PLN) increases in volume and cellularity and undergoes significant histological changes. These changes are accompanied by a major expansion in a polyclonal B cell subset with a unique surface phenotype (CD23+, CD21high, IgMhigh, IgD+, CD1d+), which is found specifically in the nodes draining affected joints. Interestingly, the same B cell population is also found in PLNs of K/BxN mice with an etiologically distinct, autoantigen-dependent form of arthritis. Here we will discuss the features of this new population in the context of arthritis and other inflammatory conditions.
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