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IL‐12 receptor regulation in IL‐12‐deficient BALB / c and C57BL / 6 mice
Author(s) -
Galbiati Francesca,
Rogge Lars,
Adorini Luciano
Publication year - 2000
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/1521-4141(200001)30:1<29::aid-immu29>3.0.co;2-7
Subject(s) - balb/c , biology , priming (agriculture) , antigen , microbiology and biotechnology , adjuvant , receptor , immunology , t cell , interleukin 4 , immune system , biochemistry , botany , germination
Abstract Immunization with protein antigen in complete Freund's adjuvant (CFA) induces Th1 cells in BALB / c and C57BL / 6 (B6) mice. Pretreatment with the same protein in soluble form induces Th2 cells in BALB / c but not in B6 mice and inhibits Th1 cell development in both. We have previously shown that inhibition of Th1 in BALB / c mice correlates with the down‐regulation of transcripts encoding the IL‐12 receptor β2 (IL‐12Rβ2) chain, which is required for IL‐12 signaling and Th1 cell development. We now demonstrate that IL‐12‐deficient BALB / c mice, when primed with antigen in CFA, mount a Th2 instead of the Th1 response which develops in wild‐type mice. Conversely, IL‐12‐deficient B6 mice fail to develop Th2 cells. Thus, a default Th2 development is induced by antigen priming in IL‐12‐deficient BALB / c but not B6 mice. IL‐12Rβ2 transcripts are still expressed in antigen‐restimulated CD4 + T cells from IL‐12‐deficient BALB / c and B6 mice and they are similarly reduced by pretreatment with soluble antigen, suggesting that intrinsic strain differences in IL‐12R regulation do not account for the differential polarization to the Th2 pathway. IL‐4 is not required for down‐regulation of IL‐12Rβ2 transcripts and inhibition of Th1 development in mice pretreated with soluble protein, as shown by their reduction in IL‐4‐deficient BALB / c mice.