Background and purpose:  Rheumatoid arthritis (RA) is an autoimmune disorder involving subsets of activated T cells, in particular T helper (Th) 1 and Th17 cells, which infiltrate and damage tissues and induce inflammation. Prostaglandin E 2 (PGE 2 ) enhances the Th17 response, exacerbates collagen‐induced arthritis (CIA) and promotes inflammatory pain. The current study investigated whether selective antagonism of the PGE 2 EP 4 receptor would suppress Th1/Th17 cell development and inflammatory arthritis in animal models of RA. Experimental approach:  Effects of PGE 2 and a novel EP 4 receptor antagonist ER‐819762 on Th1 differentiation, interleukin‐23 (IL‐23) production by dendritic cells (DCs), and Th17 development were assessed in vitro . The effect of ER‐819762 was evaluated in CIA and glucose‐6‐phosphate isomerase (GPI)‐induced arthritis models. In addition, the effects of ER‐819762 on pain were evaluated in a model of chronic inflammatory pain induced by complete Freund's adjuvant (CFA) in the rat. Key results:  Stimulation of the EP 4 receptor enhanced Th1 differentiation via phosphatidylinositol 3 kinase signalling, selectively promoted Th17 cell expansion, and induced IL‐23 secretion by activated DCs, effects suppressed by ER‐819762 or anti‐PGE 2 antibody. Oral administration of ER‐19762 suppressed Th1 and Th17 cytokine production, suppressed disease in collagen‐ and GPI‐induced arthritis in mice, and suppressed CFA‐induced inflammatory pain in rats. Conclusion and implications:  PGE 2 stimulates EP 4 receptors to promote Th1 differentiation and Th17 expansion and is critically involved in development of arthritis in two animal models. Selective suppression of EP 4 receptor signalling may have therapeutic value in RA both by modifying inflammatory arthritis and by relieving pain.