       Document 0705
 DOCN  M9630705
 TI    Modulation of immunity to Borrelia burgdorferi by ultraviolet
       irradiation: differential effect on Th1 and Th2 immune responses.
 DT    9603
 AU    Brown EL; Rivas JM; Ullrich SE; Young CR; Norris SJ; Kripke ML;
       Department of Immunology, University of Texas M.D. Anderson; Cancer
       Center, Houston 77030, USA.
 SO    Eur J Immunol. 1995 Nov;25(11):3017-22. Unique Identifier : AIDSLINE
       MED/96085170
 AB    Ultraviolet B (UVB) radiation suppresses the delayed-type
       hypersensitivity (DTH) response to alloantigen by a mechanism involving
       interleukin (IL)-10. It has been hypothesized, based on this result,
       that UV irradiation shifts the immune response from a Th1 to a Th2
       response. We tested this hypothesis using Borrelia burgdorferi (Bb) as
       an antigen under conditions where both DTH and antibody responses could
       be assessed. Mice were irradiated with a single dose of UV and then
       immunized with Bb in complete Freund's adjuvant (CFA). DTH was assessed
       by footpad challenge. At various time points thereafter, mice were bled,
       and the serum antibodies to Bb were quantitated. Only IgG1, IgG2a, and
       IgG2b were produced in response to Bb. The IgG2a and IgG2b antibody
       responses, as well as the DTH response to Bb, showed UV dose-dependent
       reductions after UV irradiation. The primary IgG1 response to Bb was
       very low and was unaffected by UV irradiation; however, the IgG1
       secondary response was elevated in UV-irradiated mice. Injection of
       anti-IL-10 antibody into UV-irradiated mice within 24 h after UV
       exposure restored the DTH response, as well as the IgG2a and IgG2b
       antibody responses. In addition, injecting recombinant murine IL-10
       mimicked some of the effects of UV radiation. Our results support the
       hypothesis that in vivo, UV irradiation down-regulates Th1 immune
       responses, while leaving Th2 responses intact, and suggest that IL-10 is
       an important mediator of this effect.
 DE    Animal  Antibodies, Bacterial/*BIOSYNTHESIS  Borrelia
       burgdorferi/*IMMUNOLOGY  Female  Hypersensitivity, Delayed/*IMMUNOLOGY
       IgG/BIOSYNTHESIS  Immunosuppression/METHODS
       Interleukin-10/*PHARMACOLOGY  Mice  Mice, Inbred C3H  Support, U.S.
       Gov't, P.H.S.  Th1 Cells/DRUG EFFECTS/*IMMUNOLOGY/RADIATION EFFECTS  Th2
       Cells/DRUG EFFECTS/*IMMUNOLOGY/RADIATION EFFECTS  *Ultraviolet Rays
       Whole-Body Irradiation  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

