Abstract
In the late 20th century, inflammatory tissue damage was thought to be driven primarily by T-helper type-1 (Th1) CD4+ T cells that secrete interleukin-2 (IL-2) and their signature cytokine, interferon-γ (IFN-γ). Over the last decade, it has become clear that other subsets of CD4+ T cells may drive immune inflammation, in particular Th17 T cells that secrete IL-17A, IL-21 and IL-22. Such Th17 T cells and their secreted products are now recognized as important drivers of central nervous system inflammation in experimental allergic encephalomyelitis,1 and may also be implicated in collagen-induced arthritis.2 These results stimulated research in other inflammatory diseases that cause injury in various tissue sites, including the liver. A paper from Yan et al.,3 working at the Shanghai Medical College, argues forcefully that the IL-17 axis is critical in the induction of liver injury in a standard model induced by intravenous injection of the plant lectin, concanavalin A (con A). However, this could be seen as an inflammatory conclusion, as other workers have tested the significance of IL-17 and its receptor in the same model of liver injury, and found it either less important than IFN-γ, or not important at all.4, 5 How can we make sense of this apparent contradiction?
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