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and IL-10 in the Regulation of Experimental Colitis
*
Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and
Laboratory of Immunology, Istituto Superiore di Sanita’, Rome, Italy
In the present study, we define the relation between TGF-
and
IL-10 in the regulation of the Th1-mediated inflammation occurring in
trinitrobenzene sulfonic acid (TNBS)-colitis. In initial studies, we
showed that the feeding of trinitrophenol-haptenated colonic
protein to SJL/J mice induces CD4+ regulatory T cells that
transfer protection from induction of TNBS-colitis, and that such
protection correlates with cells producing TGF-, not IL-10. Further
studies in which SJL/J mice were fed haptenated colonic protein, and
then administered either anti-TGF- or anti-IL-10 at the time
of subsequent TNBS administration per rectum, showed that while both
Abs abolished protection, anti-TGF- administration prevented
TGF- secretion, but left IL-10 secretion intact; whereas
anti-IL-10 administration prevented both TGF- secretion and
IL-10 secretion. Thus, it appeared that the protective effect of IL-10
was an indirect consequence of its effect on TGF- secretion. To
establish this point further, we conducted adoptive transfer studies
and showed that anti-IL-10 administration had no effect on
induction of TGF- producing T cells in donor mice. However, it did
inhibit their subsequent expansion in recipient mice, probably by
regulating the magnitude of the Th1 T cell response which would
otherwise inhibit the TGF- response. Therefore, these studies
suggest that TGF- production is a primary mechanism of
counter-regulation of Th1 T cell-mediated mucosal inflammation, and
that IL-10 is necessary as a secondary factor that facilitates TGF-
production.
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