Invasive fibroblast‐like synoviocytes in rheumatoid arthritis. Passive responders or transformed aggressors?

Abstract

Among the panoply of cells in the rheumatoid synovium, increasing attention has been directed toward non-T cell elements as potential therapeutic targets.While the precise role of T cells as initiators or perpetuators of rheumatoid arthritis (RA) is difficult to quantify, there is little disagreement that macrophages and fibroblasts play an essential part in the destructive aspects and cytokine networks of the disease.This review is designed to examine the biology of the synovial intimal fibroblast in RA and how it participates in this process.Moreover, understanding its role in the pathogenesis of RA offers a variety of novel approaches to controlling both the inflammatory and destructive aspects of arthritis. Type B synoviocytes in the intimal liningThe synovial intimal lining is the interface between the synovium and the intraarticular space.It lacks blood vessels, receiving nutrition and oxygen via a sublining vascular network (1).The lining is normally 1 or 2 layers deep and is supported by a relatively disorganized accumulation of matrix proteins rather than a true basement membrane.Lining cells do not form tight junctions with each other, but instead, are a loosely associated collection of macrophage-like type A synoviocytes and fibroblast-like type B synoviocytes.The former account for the majority of cells in both normal intima and hyperplastic RA tissue; they are derived from monocyte precursors in the bone marrow (2).