Prevention of experimental allergic encephalomyelitis by an antibody to CD45RB

CD45 is involved in the regulation of lymphocyte activation, and it has bee n demonstrated that ligation of CD45 induces apoptosis of T and B lymphocyt es, Recently anti-CD45RB antibody therapy was shown to block acute allograf t rejection in a mouse model of transplantation. Therefore, we wanted to ex amine the effects of anti-CD45RB antibody treatment on the course of an aut oimmune disorder, experimental allergic encephalomyelitis (EAE), a Th1-medi ated process. Mice immunized with myelin basic protein and treated with ant i-CD45RB antibody did not develop EAE. Histologically, there was no evidenc e of lymphocytic infiltrates in the central nervous system. T cell prolifer ation and TNF-alpha production were significantly decreased in anti-CD45RB- treated mice. Furthermore, there was a significant reduction in the product ion of other Th1 cytokines including interferon-gamma and IL-2, but not IL- 4 or IL-6. However, levels of a number of adhesion markers or markers of ac tivation such as VLA-4 and LFA-1 on T cells were no different in treated ve rsus control animals. Thus, antiCD45RB can prevent EAE and appears to do so by altering T cell proliferation and cytokine production. (C) 1998 Academi c Press.