Background
While the aetiology of rheumatoid arthritis (RA) is unknown, emerging data suggest that T cell:macrophage cell–cell interactions are critical in disease perpetuation. Cytokine/mitogen-activated CD4+ T cells or CD4+ T cells isolated directly from RA synovial fluid (SF) are known to induce tumour necrosis factor alpha (TNF-α) production by monocytes via a cell-contact-mediated mechanism. However, little is known about the ability of CD8+ cells to drive such effects.