The role of cellular immunity in systemic vasculitis
Our knowledge of the cellular component of autoimmunity (autoreactive T cells) lags far behind our knowledge of the humoral component (autoantibodies). With some rare exceptions (e.g. autonomous expansion of an autoantibody-producing B cell clone) it is probable that T cells are involved at least indirectly in providing help for the production of the better characterized autoantibodies. Although autoreactive T cells have been identified in some diseases [1-3], evidence for a direct role in pathogenesis is difficult to obtain in man. The development of knowledge concerning autoreactivity in systemic vasculitis (SV) is proceeding along familiar lines. These diseases were long suspected to have an autoimmune basis, and this suspicion was strengthened by the description of anti-neutrophil cytoplasmic antibodies (ANCA) [4]. ANCA are highly sensitive and specific for active primary systemic vasculitides involving small blood vessels (Wegener's granulomatosis (WG), microscopic polyangiitis) [5]. As well as their undoubted clinical utility it is possible that ANCA also play a role in pathogenesis [6]. Following this description of humoral autoreactivity in SV, it was natural to ask whether autoreactive T cells were also present.