Recruitment of Neutrophils Mediated by V{gamma}2 {gamma}{delta} T Cells Deteriorates Liver Fibrosis Induced by Schistosoma japonicum Infection in C57BL/6 Mice [Host Response and Inflammation]

Conventional adaptive T cell responses contribute to the pathogenesis of Schistosoma japonicum infection, leading to liver fibrosis. However, the role of gamma-delta () T cells in this disease is less clear. T cells are known to secrete interleukin-17 (IL-17) in response to infection, exerting either protective or pathogenic functions. In the present study, mice infected with S. japonicum are used to characterize the role of T cells. Combined with the infection of S. japonicum, an extremely significant increase in the percentage of neutrophils in the CD45⁺ cells was detected (from approximately 2.45% to 46.10% in blood and from 0.18% to 7.34% in spleen). Further analysis identified two different T cell subsets that have different functions in the formation of granulomas in S. japonicum-infected mice. The V1 T cells secrete gamma interferon (IFN-) only, while the V2 T cells secrete both IL-17A and IFN-. Both subtypes lose the ability to secrete cytokine during the late stage of infection (12 weeks postinfection). When we depleted the V2 T cells in infected mice, the percentage of neutrophils in blood and spleen decreased significantly, the liver fibrosis in the granulomas was reduced, and the level of IL-17A in the serum decreased (P < 0.05). These results suggest that during S. japonicum infection, V2 T cells can recruit neutrophils and aggravate liver fibrosis by secreting IL-17A. This is the first report that a subset of T cells plays a partial role in the pathological process of schistosome infection.

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