Figure 5.

Signalling via tumour necrosis factor receptor 1 (TNFR1) enhances prostaglandin E₂ (PGE₂) production, which contributes to T-cell regulation. Wild-type (WT) or TNFR1^−/− bone-marrow-derived macrophages (BM-Mϕ) were co-cultured with OT-II T cells and ovalbumin (OVA) peptide for 72 hr. In some experiments the pan-cyclo-oxygenase (COX) inhibitor indomethacin or the COX-2-specfic inhibitor SC-256 was added. In other experiments, PGE₂ was added. PGE₂ concentration (a) and proliferation (b) of co-cultures containing WT Mϕ (black bars) or TNFR1^−/− Mϕ (grey lines) treated with COX inhibitors was measured. Proliferation (top) and nitric oxide (NO) production (bottom) were measured from co-cultures with WT Mϕ (black bars, left-hand graphs) or TNFR1^−/− (grey bars, right-hand graph) with PGE₂ added at a range of concentrations (c). These data are representative of two independent experiments. *Significantly different to control WT MϕP < 0·05.