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The bullseye synapse formed between CD4 + T‐cell and staphylococcal enterotoxin B‐pulsed dendritic cell is a suppressive synapse in T‐cell response
Author(s) -
Lin Wei,
Fan Zhichao,
Suo Yuanzhen,
Deng Yuting,
Zhang Min,
Wang Jiyang,
Wei Xunbin,
Chu Yiwei
Publication year - 2015
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2014.76
Subject(s) - immunological synapse , cytotoxic t cell , t cell , il 2 receptor , synapse , antigen presenting cell , microbiology and biotechnology , jurkat cells , chemistry , antigen , cd28 , immune system , biology , immunology , t cell receptor , biochemistry , neuroscience , in vitro
The immunological synapse (IS) is a supermolecular activation cluster formed between T cells and antigen‐presenting cells. Although diverse IS structures have been reported, the function of the IS in T‐cell activation remains unclear. Here, we found that the bullseye IS, one of IS types at the interface of CD4 + T cells and staphylococcal enterotoxin B‐pulsed dendritic cells, suppressed CD4 + T‐cell activation, whereas multifocal IS, another synapse type, stimulated CD4 + T‐cell activation. Consistent with these results, bullseye IS formation was accompanied by a low‐level calcium response in T cells and a loss of T‐cell receptor signalling molecules from the synapse, whereas multifocal IS exhibited the opposite. Furthermore, we found that CD4 + CD25 + regulatory T cells (T regs ) more efficiently formed bullseye IS and promoted bullseye IS formation in CD4 + CD25 − T cells. Cytotoxic T‐lymphocyte antigen‐4 (CTLA‐4), an inhibitory molecule expressed continuously on T regs , was localised in bullseye IS. Moreover, blocking CTLA‐4 reduced the percentage of bullseye IS formation and promoted T‐cell activation. Our data thus indicate that bullseye IS formation is mediated by CTLA‐4, and may negatively control T‐cell activation as a suppressive synapse.