Hapten-induced colitis associated with maintained Th1 and inflammatory responses in IFN-gamma receptor-deficient mice.
作者： Luisa Camoglio , Anje A. te Velde , Anita de Boer , Fibo J. ten Kate , Manfred Kopf
DOI: 10.1002/(SICI)1521-4141(200005)30:5<1486::AID-IMMU1486>3.0.CO;2-8
关键词:
摘要: IFN-gamma is a potent pro-inflammatory cytokine thought to be involved in the pathogenesis of Crohn's disease. To further define role intestinal inflammation, we studied effects intra-colonic 2,4,6-trinitrobenzene sulfonic acid (TNBS) instillation mice with functionally inactivated receptor 1 (IFN-gammaR1(- / -)). Our results indicate that not necessary for induction hapten-induced colitis: after TNBS administration both wild-type and IFN-gammaR1(- -) lost body weight, histological features TNBS-induced colitis were comparable. Colons contained greater number cells, represented by macrophages CD4(+) T cells; caudal lymph node cells produced more TNF-alpha upon stimulation vitro. Moreover, IL-18 IL-12 p40 RNA levels comparably up-regulated treatment mice. These findings demonstrate dispensable development colitis. Importantly, production Th1 cytokines (e. g. TNF-alpha) lymphocytes was enhanced rather than decreased IFNgammaR1(- no evidence default Th2 development.
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