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The role of IL‐4, IL‐10, and TNF‐ α in the immune suppression induced by ultraviolet radiation
Author(s) -
Rivas Jorge M.,
Ullrich Stephen E.
Publication year - 1994
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.56.6.769
Subject(s) - immune system , tumor necrosis factor alpha , antigen , immunology , antibody , interleukin , biology , interleukin 4 , cytokine , microbiology and biotechnology
Cytokines produced by keratinocytes play an essential role in the induction of immune suppression following ultraviolet (UV) exposure. Using antibodies specific for either interleukin‐10 (IL‐10) or tumor necrosis factor α (TNF‐ α ), we present evidence indicating that IL‐10 suppresses delayed‐type hypersensitivity (DTH) but not contact hypersensitivity (CHS), whereas TNF‐ α suppresses CHS but not DTH following UV exposure. UV exposure also activates antigen‐specific suppressor T cells. To determine whether the antigen‐specific CD4 + T cells that transfer suppression in this system mediate their suppressive effect by releasing IL‐4 or IL‐10, we transferred UV Ts into normal mice that were then injected with either anti‐IL‐4 or anti‐IL‐10 antibody. Both anti‐ IL‐4 and anti‐IL‐10 blocked the ability of UV Ts cells to suppress DTH in the recipient animals. When UV Ts that suppress CHS were transferred into normal recipients, however, neither antibody was able to block the UV Ts activity. These findings suggest that UV Ts suppress DTH by secreting IL‐4 and IL‐10 and appear to act like Th2 cells. Because anti‐IL‐4 and anti‐IL‐10 did not block the activity of the UV Ts that regulate contact hypersensitivity, their effects appear to be mediated by a different mechanism. J. Leukoc. Biol. 56: 769–775; 1994.