IL-22-Dependent Attenuation of T Cell-Dependent (ConA) Hepatitis in Herpes Virus Entry Mediator Deficiency
作者： Christian Wahl , Ursula Maria Wegenka , Frank Leithäuser , Reinhold Schirmbeck , Jörg Reimann
关键词: Population 、 Proinflammatory cytokine 、 Natural killer T cell 、 Cell 、 Biology 、 Interleukin 22 、 T cell 、 Molecular biology 、 Immunology 、 Dendritic cell 、 Hepatitis
摘要: Coinhibitors and costimulators control intrahepatic T cell responses that trigger acute hepatitis. We used the ConA-induced hepatitis model in mouse to test if coinhibitor herpes virus entry mediator (HVEM) modulates hepatitis-inducing responses. Compared with ConA-injected, wild-type (wt) C57BL/6 (B6) mice, HVEM-deficient (HVEM−/−) B6 mice showed lower serum transaminase levels proinflammatory IFN-γ, but higher protective IL-22 an attenuated liver histopathology. The type I invariant NKT population initiates this was reduced HVEM−/− their surface phenotype similar of untreated or ConA-treated wt controls. In response mitogen injection, cells from produced vivo more amounts IFN-γ IL-4 than Bone marrow chimeras HVEM deficiency nonparenchymal population, not parenchymal mediated course dendritic cell- cell-dependent ConA is efficiently by its Ab-mediated neutralization aggravated mice. Hence, expression promotes pathogenic, Th1 down-modulates
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