Cutting edge: Attenuated experimental autoimmune encephalomyelitis in Eta-1/osteopontin-deficient mice

Recent studies indicate that early T lymphocyte activation 1 (Eta-1), also known as osteopontin, is a cytokine contributing to the development of Th1 immunity. In the present report, the role of Eta-1 in experimental autoimmune encephalomyelitis (EAE), a disease associated with Th1 immunity, was examined by analysis of disease progression in Eta-l-deficient (Eta-1(-/-)) mice. Although incidence and onset of peptide-induced EAE were found to be similar in Eta-1(-/-) and Eta-1(+/+) mice, Eta-1(-/-) mice displayed significantly lower mean maximal clinical score and faster recovery without spontaneous relapses. Accordingly, decreased inflammatory infiltration and demyelination were observed in the spinal cords of Eta-1(-/-) mice. Furthermore, in comparison to Eta-1(+/+), Eta-1(-/-) CD4(+) T cells had reduced expression of IFN-gamma and TNF-alpha upon ex vivo restimulation. Taken together, these results suggest that Eta-1 may sustain autoimmune responses by assisting in maintenance of Th1 immunity during EAE.