Background
Previous studies in this laboratory have highlighted the importance of the proinflammatory cytokine tumour necrosis factor alpha (TNF-α) in the pathogenesis of rheumatoid arthritis (RA) and suggested a role for bystander-activated lymphocytes in its chronic production in the RA joint. Normal peripheral blood (PB) lymphocytes cultured in the presence of a 'cocktail' of inflammatory cytokines (IL-2/IL-6/TNF-α) generated effector cells (TCK) capable of inducing both immunoglobulin production by B cells [1] and TNF-α production by monocytes in a contact-dependent manner. This was in contrast to lymphocytes activated antigen dependently, via the T-cell receptor (TTCR), which induced production of both TNF-α and the anti-inflammatory cytokine IL-10 [2, 3]. Lymphocytes isolated from the RA synovial membrane exhibited contact-dependent cytokine induction properties similar to TCK, not TTCR, cells [4].