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CD4+ T cells use IFN‐γ, not IL‐17, to drive neutrophil‐mediated liver damage in murine autoimmune hepatitis

Autoimmune hepatitis (AIH) is a poorly understood disease caused by an immune‐mediated attack on hepatocytes. BALB/c‐TGF‐β1−/− mice spontaneously develop fulminant AIH that recapitulates important features of the human disease. Liver disease is dependent upon both CD4+ T cells and IFN‐γ. Intracellular cytokine analysis as well as cell subset depletion showed that CD4+ T cells, but not CD8+ T cells or NK cells, are the relevant source of IFN‐γ in this model system. Histological examination of TGF‐β1−/− livers revealed an abundance of neutrophils, supported by microarray analysis showing increased expression of neutrophil‐associated gene products. Liver neutrophilia was dependent upon the CD4+ T cell subset as well as on the Th1 cytokine IFN‐γ. Interestingly, TGF‐β1−/− liver CD4+ T cells produced abundant IFN‐γ, but no detectable IL‐17. The relevance of the neutrophil subset for pathology was confirmed directly, as depletion of neutrophils using a subsetspecific monoclonal antibody protected TGF‐β1−/− mice from liver disease. Thus AIH in TGF‐β1−/− mice is driven by a CD4+ Th1 – IFN‐γ – neutrophil pathway, with no role for IL‐17.