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PAR-2 deficient CD4+ T cells exhibit downregulation of IL-4 and upregulation of IFN-gamma after antigen challenge in mice.
Authors:Michitaka Shichijo  Shinichi Kondo  Mina Ishimori  Shinichi Watanabe  Heidi Helin  Tsugiko Yamasaki  Mary E Stevens  Florian Gantner  Kevin B Bacon
Affiliation:Respiratory Diseases Research, Research Center Kyoto, Bayer Yakuhin Ltd, Kyoto, Japan. michitaka.shichijou@shionogi.co.jp
Abstract:BACKGROUND: To investigate the functional role of protease activated receptor (PAR) -2 in T lymphocytes, we analyzed TCR-mediated inflammatory cytokine production using PAR-2 deficient (KO) and wild type (WT) mice. METHODS: Production of serum IgE and cytokines by spleen CD4+ T cells was determined in OVA-sensitized and OVA-challenged mice of PAR-2 KO in contrast to WT mice. Phosphorylation of JNK1 and 2 was determined by Western blotting. RESULTS: A reduction in serum levels of IgE and IL-4 production by splenic CD4+ T cells from OVA-sensitized and OVA-challenged KO mice compared to WT mice was observed. By contrast, IFN-gamma production was upregulated after antigen stimulation in KO mice. Anti-CD3-mediated phosphorylation of JNK1 was upregulated in splenic CD4+ T cells from KO mice compared to WT mice. CONCLUSIONS: PAR-2 participates in the regulation of T cell cytokine production that may be caused by modulation of JNK1 phosphorylation.
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