Prevention of experimental allergic encephalomyelitis by an antibody to CD45RB

Citation
J. Schiffenbauer et al., Prevention of experimental allergic encephalomyelitis by an antibody to CD45RB, CELL IMMUN, 190(2), 1998, pp. 173-182
Citations number
32
Categorie Soggetti
Immunology
Journal title
CELLULAR IMMUNOLOGY
ISSN journal
00088749 → ACNP
Volume
190
Issue
2
Year of publication
1998
Pages
173 - 182
Database
ISI
SICI code
0008-8749(199812)190:2<173:POEAEB>2.0.ZU;2-0
Abstract
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.