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Effects of monoclonal antibodies directed at cell surface molecules on murine experimental autoimmune uveoretinitis
K Ando1, Y Fujino, M Mochizuki
1Department of Ophthalmology, Tokyo University School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Background:
To elucidate the immunopathogenic mechanism of endogenous uveitis, the effects of monoclonal antibodies to molecules involved in the immune response were studied in murine experimental autoimmune uveoretinitis (EAU).
Methods:
Monoclonal antibodies to CD4, CD8, Ia(k), Ia(d), lymphocyte function-associated antigen-1 (LFA-1), and intercellular adhesion molecule-1 (ICAM-1) were used in this study. The monoclonal antibodies were added in the culture of lymph node cells from B10.BR mice(H-2(K)) immunized with interphotoreceptor retinoid-binding protein (IRBP) and the inhibition of proliferative response was measured. In vivo, IRBP-immunized mice were treated with a high dose of the antibody, and the EAU induction was examined both clinically and pathologically.
Results:
Proliferative response of IRBP-sensitized lymph node cells was inhibited strongly by anti-CD4 or anti-LFA-1 monoclonal antibody and moderately by anti-Ia(k) or anti-ICAM-1 monoclonal antibody. In contrast, no inhibitory effect of anti-CD8 or anti-Ia(d) monoclonal antibody was observed. In vivo treatment with anti-CD4 monoclonal antibody inhibited development of EAU in a dose-dependent manner, while in vivo treatment with other monoclonal antibodies did not cause significant suppression of EAU.
Conclusions:
CD4, Ia, LFA-1, and ICAM-1 molecules play important roles in the antigen-specific immune response of lymphocytes. However, in in vivo treatment with monoclonal antibodies to these molecules, only anti-CD4 monoclonal antibody had a strong inhibitory effect on the development of EAU.