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CD24 aggravates acute liver injury in autoimmune hepatitis by promoting IFN-γ production by CD4+ T cells.

Abstract：

:The T-cell-mediated immune response is implicated in many clinical hepatic injuries, such as autoimmune hepatitis and acute virus hepatitis. CD24 is widely expressed by different immune cells and plays an important role in the pathogenesis of many autoimmune diseases. However, the role of CD24 in T-cell-mediated liver injury has not been elucidated until now. Here we showed that CD24 deficiency protects mice from concanavalin A (ConA)-induced fulminant liver injury by reducing serum interferon-γ (IFN-γ) levels. CD24 expression by hepatic T cells was markedly increased following ConA challenge. Moreover, decreased IFN-γ production by hepatic CD4+ T cells in CD24-deficient mice was detected, which was correlated with downregulated phosphorylation of STAT1 in hepatic tissue. In vitro experiments also supported the conclusion that CD24 deficiency impaired IFN-γ production by CD4+ T cells following ConA, CD3/CD28 and phorbol myristate acetate/ionomycin stimulation. Our study suggests that CD24 deficiency confers hepatoprotection by decreasing CD4+ T-cell-dependent IFN-γ production in vivo, which suggests that CD24 might be a potential target molecule for reducing clinical hepatitis.

journal_name

Cell Mol Immunol

journal_title

Cellular & molecular immunology

authors

Zheng C,Yin S,Yang Y,Yu Y,Xie X

doi

10.1038/cmi.2016.57

subject

Has Abstract

pub_date

2018-03-01 00:00:00

pages

260-271

issue

3

eissn

1672-7681

issn

2042-0226

pii

cmi201657

journal_volume

15

pub_type

杂志文章

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