ANTIBODIES TO THE COSTIMULATORY MOLECULE CD86 INTERFERE WITH ULTRAVIOLET RADIATION-INDUCED IMMUNE SUPPRESSION

Citation
Se. Ullrich et al., ANTIBODIES TO THE COSTIMULATORY MOLECULE CD86 INTERFERE WITH ULTRAVIOLET RADIATION-INDUCED IMMUNE SUPPRESSION, Immunology, 94(3), 1998, pp. 417-423
Citations number
27
Categorie Soggetti
Immunology
Journal title
ISSN journal
00192805
Volume
94
Issue
3
Year of publication
1998
Pages
417 - 423
Database
ISI
SICI code
0019-2805(1998)94:3<417:ATTCMC>2.0.ZU;2-M
Abstract
Although almost all of the energy contained within the ultraviolet (UV ) wavelengths of solar radiation is absorbed within the epidermis and upper layers of the dermis, UV irradiation can suppress the immune res ponse to antigens introduced at distant, non-irradiated body sites. Th e production of immune modulatory cytokines, such as interleukin-10 (I L-10), by UV-irradiated keratinocytes and its effect on T helper type 1 (Th1)/Th2-cell balance are thought to play a major role in the induc tion of systemic immune suppression. Because it is suggested that cost imulatory molecules, such as CD80 and CD86, differentially stimulate T h1 and Th2 cells we wished to investigate the role of these costimular ory molecules in the activation of immune suppression. We injected UV- irradiated mice with monoclonal antibodies to CD80 and CD86 and asked what effect, if any, this would have on UV-induced immune suppression. Anti-CD86, but not anti-CD80 or control rat IgG, blocked UV-induced i mmune suppression. Moreover, monoclonal anti-CD86 blocked the inductio n of suppressor T cells normally found in the spleens of the UV-irradi ated mice. Monoclonal anti-CD86 also reversed the UV-induced impairmen t of systemic antigen-presenting cell function. IL-10 was delectable i n the serum of UV-irradiated mice as compared with normal controls, an d injecting UV-irradiated mice with anti-CD86, but not anti-CD80 or co ntrol rat IgG, blocked the secretion of IL-10 into the serum. We propo se that UV exposure favours costimulation by CD86, which enhances the production of serum IL-10, thus suppressing Th1-cell-mediated immune r eactions.