Disruption of TIM-4 in dendritic cell ameliorates hepatic warm IR injury through the induction of regulatory T cells

Molecular Immunology
Ji LiHuanqiu Liu

Abstract

Hepatic ischaemia reperfusion (IR) injury results from the infiltration of multiple immune cells especially dendritic cells (DC). T-cell immunoglobulin-domain and mucin-domain 4 (TIM-4) is a type I cell-surface glycoprotein which is extensively expressed on antigen presenting cells (APC) like DC and macrophages. TIM-4 has been demonstrated to be implicated in mucosal allergy, skin allograft rejection and tumour-immune tolerance. However, the role of TIM-4 expressed on DC in hepatic IR injury remains largely unknown. In the present study, we aimed to investigate whether and how DC expressed TIM-4 was involved in hepatic IR injury. With segmental hepatic warm ischaemia mice models, we demonstrated that promoted DC infiltration and increased TIM-4 expression were induced by hepatic IR. Blockade of TIM-4 by anti-TIM-4 mAb (0.35mg/mouse) markedly ameliorated hepatic injury and reduced inflammatory cytokine secretion. Furthermore, in a DC:CD4+ T cell co-culture system, blockade of TIM-4 on DC significantly inhibited T helper-2 cell differentiation and facilitated induced CD4+ CD25+ Foxp3+ T regulatory cell (iTreg) expansion. Interleukin-4 (IL-4)/signal transducer and activator of transcription 6 (Stat 6) signalling was shown to be im...Continue Reading

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Citations

Aug 18, 2016·Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology·L-H MoP-C Yang
Mar 9, 2017·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Yakun WuJianping Gong
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Sep 28, 2017·International Journal of Molecular Medicine·Tianyong HuZhiqiang Liu
May 18, 2021·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Ming NiYuan Zhai

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