Temporal arteritis (TA) is an acute vasculitis characterised by destruction of arterial architecture following infiltration of the arterial wall by macrophages, giant cells and lymphocytes. Using immunohistochemical techniques, tumour necrosis factor (TNF) was demonstrated in up to 60% of the cells in all areas of inflamed arteries. More cells staining for TNF were detected in the intima and media of inflamed vessels than control uninflamed arteries (P < 0.003 and P < 0.001, respectively). In TA, TNF was localised to giant cells and macrophages, suggesting that its predominant source is from the monocyte lineage, but, occasionally, TNF staining was found in areas infiltrated by T cells. Many endothelial cells also contained TNF, but there were no differences between the number of endothelial cells staining in inflamed and normal blood vessels. Of the two TNF receptors, the p75 receptor was sparsely represented in the inflamed vessels in TA. By comparison, the p55 receptor was widely detected on endothelial cells and infiltrating mononuclear cells close to the internal elastic lamina (IEL). Endothelial cells from normal vessels also stained for both TNF receptors, but normal smooth muscle cells in the vessel media expressed the p55 receptor, indicating that they are capable of responding to locally secreted TNF. Localisation of TNF receptors and TNF in close proximity to the IEL suggests that TNF could be involved in the leucocyte infiltration and arterial wall destruction characteristic of TA.