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Angiotensin II contributes to intratumoral immunosuppressionvia induction of PD-L1 expression in non-small cell lung carcinoma.

Abstract：

:The formation of an immunosuppressive microenvironment and up-regulation of PD-L1 protein are the main causes of tumor immune escape. Previous reports suggest that Angiotensin II (Ang II) can modulate the immune status of tumor microenvironment in non-small cell lung cancer (NSCLC), but the underlying mechanism remains not fully understood. Here we demonstrated that AngII treatment causes the reduction of intratumoral infiltrating CD4 T lymphocytes in tumor-bearing mice, increases the accumulation of immunosuppressive granulocytes and TAMs in tumor tissue, and upregulates the expression levels of immunosuppressive marker genes. In addition, AngII/AGTR1 axis triggers cell PD-L1 expression through a mechanism involving increases in PD-L1 mRNA stability by human antigen R (HuR), an AU-rich element (ARE)-binding protein. Collectively, AngII/AGTR1 signaling promotes the tumor immunosuppressive microenvironment by upregulating PD-L1 in NSCLC, the mechanism of which is largely accounted by HuR-mediated PD-L1 mRNA stabilization.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Yang K,Zhou J,Chen Y,Chen Y,Chen L,Zhang P,Ma L,Jiang Z,Bian J,Yin W

doi

10.1016/j.intimp.2020.106507

subject

Has Abstract

pub_date

2020-07-01 00:00:00

pages

106507

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(20)30254-X

journal_volume

84

pub_type

杂志文章

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