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.