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Annexin V expression on CD4 + T cells with regulatory function
Author(s) -
Bollinger AnnaLena,
Bollinger Thomas,
Rupp Jan,
Shima Kensuke,
Gross Natalie,
Padayachy Laura,
Chicheportiche Rachel,
Puga Yung Gisella L.,
Seebach Jörg Dieter
Publication year - 2020
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.13140
Subject(s) - annexin a5 , cytotoxic t cell , il 2 receptor , t cell , biology , cd38 , microbiology and biotechnology , cd28 , annexin , immune system , antigen , jurkat cells , immunology , in vitro , flow cytometry , biochemistry , stem cell , cd34
Summary Regulatory T (Treg) cells induce immunologic tolerance by suppressing effector functions of conventional lymphocytes in the periphery. On the other hand, immune silencing is mediated by recognition of phosphatidylserine (PS) on apoptotic cells by phagocytes. Here we describe expression of the PS‐binding protein Annexin V (ANXA5) in CD4 + CD25 hi Treg cells at the mRNA and protein levels. CD4 + ANXA5 + T cells constitute about 0·1%–0·6% of peripheral blood CD3 + T cells, exhibit co‐expression of several Treg markers, such as Forkhead box P3, programmed cell death protein‐1, cytotoxic T‐lymphocyte antigen‐4 and CD38. In vitro , ANXA5 + Treg cells showed enhanced adhesion to PS + endothelial cells. Stimulated by anti‐CD3 and PS + syngeneic antigen‐presenting cells CD4 + ANXA5 + T cells expanded in the absence of exogenous interleukin‐2. CD4 + ANXA5 + T cells suppressed CD4 + ANXA5 − T‐cell proliferation and mammalian target of rapamycin phosphorylation, partially dependent on cell contact. CD4 + ANXA5 + T‐cell‐mediated suppression was allo‐specific and accompanied by an increased production of anti‐inflammatory mediators. In vivo , using a model of delayed type hypersensitivity, murine CD4 + ANXA5 + T cells inhibited T helper type 1 responses. In conclusion, we report for the first time expression of ANXA5 on a subset of Treg cells that might bridge classical regulatory Treg function with immune silencing.