Suppression and prevention of adjuvant arthritis in rats by a monoclonal antibody to the α/β T cell receptor

Abstract

Adjuvant arthritis (AA) in rats is an experimentally induced autoimmune disease mediated by T lymphocytes specific for Mycobacterium tuberculosis. We raised the question whether T cells carrying the γ/δ Tcell receptor (TcR), reactive or not to mycobacterial antigens, are involved in the pathogenesis of AA. For this purpose, T cells bearing the TcR α/β were depleted from circulation by treatment with a monoclonal antibody against the rat TcR α/β (R73). This treatment efficiently suppressed existing disease. Even more efficient was pretreatment with R73 from birth, which prevented AA induction completely. In these α/β⁺ T cell‐depleted animals an elevated level of α/β⁻ T cells (about 15% vs. 1% in normal rats) was evident, which was not significantly increased by Mycobacterium tuberculosis injection. We found no positive evidence that γ/δ⁺ T cells do contribute to AA induction. Moreover, treatment with an anti‐TcR α/β monoclonal antibody may be very efficient in treatment of Tcell‐mediated autoimmune diseases.