International Immunology, Vol 10, 807-814, Copyright © 1998 by Oxford University Press
LV Rizzo, H Xu, CC Chan, B Wiggert and RR Caspi
The role of IL-10 in the regulation of ocular autoimmune disease was
studied in experimental autoimmune uveoretinitis (EAU) elicited in mice by
immunization with the retinal antigen interphotoreceptor retinoid binding
protein. IL-10-deficient mice were susceptible to EAU, indicating that
pathogenesis can occur without presence of IL-10. Treatment of normal mice
with IL-10 for 5 days after uveitogenic immunization ameliorated subsequent
EAU scores, and down-regulated antigen-specific production of tumor
necrosis factor-alpha and IFN- gamma. A concomitant treatment with IL-4
further reduced disease, and resulted in emergence of antigen-specific IL-4
and IL-10 production, as well as in enhancement of the IgG1 antibody
isotype. IL-4 by itself was not protective. Only IL-10, but not IL-4, was
able to inhibit the function of differentiated uveitogenic T cells in
culture. Expression of mRNA for Th1 and Th2 cytokines in the eye during the
course of EAU showed that while a Th1 pattern predominated early, IL-10
mRNA expression coincided with down-regulation of the Th1 response and
resolution of EAU. Systemic neutralization of IL-10 during the expression
phase of EAU resulted in elevated disease scores. Our results suggest that
endogenous IL-10 limits expression of EAU and may play a role in the
natural resolution of disease. The data further suggest that exogenous
IL-10 may be useful in therapeutic control of autoimmune uveitis. While
IL-10 by itself is sufficient to suppress Th1 effector development and
function, a concomitant administration of IL-4 is required to shift the
autoimmune response towards a non-pathogenic Th2 pathway.
ARTICLES
IL-10 has a protective role in experimental autoimmune uveoretinitis
Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892-5897, USA.
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