γδ T cells are indispensable for interleukin‐23‐mediated protection against Concanavalin A‐induced hepatitis in hepatitis B virus transgenic mice

• DOI: 10.1111/imm.12712
• Publication Date: 2017-01-16T20:57:13Z
• Authors: Ziyu Meng; Jingya Wang; Yifang Yuan; Guangchao Cao; Shuobing Fan; Chao Gao; Li Wang; Zheng Li; Xiaoli Wu; Zhenzhou Wu; Liqing Zhao; Zhinan Yin
• Keywords: Mice, Knockout; Hepatitis B virus; Hepatitis B Surface Antigens; T-Lymphocytes; Interleukin-17; Mice, Transgenic; Receptors, Antigen, T-Cell, gamma-delta; Hepatitis B; Interleukin-23; 3. Good health; Mice, Inbred C57BL; Interferon-gamma; Mice; Necrosis; 03 medical and health sciences; 0302 clinical medicine; Liver; Concanavalin A; Animals; Humans; Cells, Cultured

Hepatitis B virus surface antigen (HBsAg) carriers are highly susceptible to liver injury triggered by environmental biochemical stimulation. Previously, we have reported an inverse correlation between γδ T cells and damage in patients with hepatitis (HBV). However, whether play a role regulating the hypersensitivity of HBsAg stimulation-induced is unknown. In this study, using HBV transgenic (HBs-Tg) HBs-Tg T-cell receptor-δ-deficient (TCR-δ-/- ) mice, found that mice genetically deficient exhibited more severe upon Concanavalin A (Con A) treatment, as indicated substantially higher serum alanine aminotransferase levels, further elevated interferon-γ (IFN-γ) levels extensive necrosis. deficiency resulted IFN-γ CD4+ but not natural killer or cells. The depletion neutralization reduced HBs-Tg-TCR-δ-/- similar extent. Further investigation revealed showed enhanced interleukin-17 (IL-17) signature. administration exogenous IL-23 IL-17A production from Vγ4 ameliorated mice. summary, our results demonstrated played protective restraining Con A-induced inhibiting indispensable for IL-23-mediated protection against These provided potential therapeutic approach treating damage.