Objective: To investigate the expression of OX40 on CD(4)(+) T cells in patients with ulcerative colitis (UC) and the role of OX40/OX40L interaction for the cytokine production of lamina propria (LP)-CD(4)(+) T cells from UC.

Methods: LP-CD(4)(+) T cells were purified. The expression of OX40 molecule was measured with FACS. LP-CD(4)(+) T cells were cultured with different stimuli and proliferation was assessed. The cytokines concentrations of the culture supernatant were detected.

Results: No difference of the OX40 expression was observed among the CD(4)(+) T cells from peripheral blood (PB) of UC patients, LP of non-inflammatory colonic tissue in UC patients and control PB. However, the expression of OX40 was significantly higher on LP-CD(4)(+) T cells from inflammatory colonic tissue in UC patients. In vitro culture with antigen presenting cells, the levels of IFNgamma and TNFalpha secreted by LP-CD(4)(+) T cells from the inflammatory colonic tissue were significantly higher than those from the non-inflammatory colonic tissue (both P < 0.01). The levels of IFNgamma and TNFalpha secreted by LP-CD(4)(+) T cells from the inflammatory colonic tissue were further increased by anti-OX40 MoAb stimulation, but suppressed significantly by adding anti-OX40L MoAb (compared with non stimulation, P < 0.01, respectively). The IFNgamma and TNFalpha secretion of the LP-CD(4)(+) T cells from the non-inflammatory colonic tissue were not significantly different with and without anti-OX40 or anti-OX40L MoAbs stimulation. IL-4 and IL-10 produced by LP-CD(4)(+) T cells from the inflammatory or non-inflammatory colonic tissue were not significantly changed when adding different stimuli.

Conclusions: OX40 is highly expressed on LP-CD(4)(+) T cells from inflammatory colonic tissue in patients with UC. Anti-OX40L MoAb can inhibit the proinflammatory cytokines secreted by these cells. It is indicated that OX40(+) T cells are involved in the immunopathological process in UC and blockage of the interaction of OX40 and OX40L is a new strategy to be considered for the treatment of the disease.