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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Peptidoglycan-linked protein A promotes T cell-dependent antibody expansion during Staphylococcus aureus infection
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Peptidoglycan-linked protein A promotes T cell-dependent antibody expansion during Staphylococcus aureus infection

机译：Peptidoglycan-linked protein A promotes T cell-dependent antibody expansion during Staphylococcus aureus infection

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摘要

A hallmark of Staphylococcus aureus disease in humans is persistent infections without development of protective immune responses. Infected patients generate V(H)3 plasmablast expansions and increased V(H)3 idiotype Ig; however, the mechanisms for staphylococcal modification of immune responses are not known. We report here that S. aureus-infected mice generate VH3 antibody expansions via a mechanism requiring MHC-restricted antigen presentation to CD4(+) T cells and staphylococcal protein A (SpA), a cellwall-anchored surface molecule that binds Fc gamma and V(H)3 variant heavy chains of Ig. VH3 expansion occurred with peptidoglycan-linked SpA from the bacterial envelope but not with recombinant SpA, and optimally required five tandem repeats of its Ig-binding domains. Signaling via receptor-interacting serine/threonine protein kinase 2 (RIPK2) was essential for implementing peptidoglycan-linked SpA superantigen activity. V(H)3 clan IgG from S. aureus-infected or SpA-treated animals was not pathogen-specific, suggesting that SpA cross-linking of V(H)3 idiotype B-cell receptors and activation via attached peptidoglycan are the determinants of staphylococcal escape from adaptive immune responses.

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