Introduction

Rheumatoid arthritis (RA) is a chronic inflammatory disease with autoimmune features chiefly affecting the synovial joints. In common with many other autoimmune diseases, there is emerging evidence to suggest that susceptibility to RA is determined by several genes (Wordsworth & Bell, 1991). However, despite the evidence of a genetic predisposition (in particular HLA-DR4 or HLA-DR1), it is clear that the genetic component is probably relatively small since concordance rates in monozygotic twins are no more than 30%, suggesting that other factors are involved (Wordsworth & Bell, 1991; Rigby et al., 1991; Silman, 1991).

The target tissue for the autoimmune and inflammatory response in RA is the synovial joint. In healthy individuals, the synovial membrane is virtually acellular, but in RA it is infiltrated extensively by large numbers of cells from the blood, including activated T cells, macrophages and plasma cells (Janossy et al., 1981; Fϕrre, Dobloug & Natvig, 1982; Burmester et al., 1982). In addition, there is proliferation of fibroblasts in the lining layer of the synovial membrane. Many of these infiltrating and resident cells including endothelial cells, fibroblasts and T cells normally express little, if any, HLA class II antigens but are activated in the RA synovium and express abundant HLA class II antigens (Førre et al., 1982; Klareskog et al., 1982; Burmester et al., 1987). These cells may act as antigen-presenting cells and be involved in the stimulation of autoreactive T cells.