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Contrasting roles of IL-12p40 and IL-12p35 in the development of hapten-induced colitis

✍ Scribed by Luisa Camoglio; Nicole P. Juffermans; Maikel Peppelenbosch; Anje A. te Velde; Fibo J. ten Kate; Sander J. H. van Deventer; Manfred Kopf

Publisher: John Wiley and Sons
Year: 2002
Tongue: English
Weight: 191 KB
Volume: 32
Category: Article
ISSN: 0014-2980
DOI: 10.1002/1521-4141(200201)32:1<261::aid-immu261>3.0.co;2-x

No coin nor oath required. For personal study only.

✦ Synopsis

IL-12(p70), a heterodimer composed of two subunits (p35 and p40), is a key cytokine for Th1 mediated inflammatory responses. We dissected the role of IL-12 in the development of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis by studying mice deficient in IL-12p40, IL-12p35, or IL-12R g 1. TNBS-treated IL-12R g 1 -/-and IL-12p35 -/-mice developed only a mild disease associated with low level IL-18 expression in IL-12p35 -/-mice. In contrast, IL-12p40 -/-mice developed more severe colitis than wild-type mice associated with high level colonic IL-18 expression. Administration of IL-12p40 neutralizing mononuclear antibody dramatically increased pathology in IL-12p35 -/-mice similar to disease scored in IL-12p40 -/-mice. Numbers of IFN-+ -producing cells infiltrating the lamina propria were comparably augmented in the different groups of IL-12-mutant and wild-type mice. These results demonstrate that IL-12p40, in contrast to IL-12p70, inhibits TNBS-induced colitis and IL-18 expression independent of IFN-+ .

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