Lipoteichoic acid anchor triggers Mincle to drive protective immunity against invasive group A Streptococcus infection

T Imai; T Matsumura; S Mayer-Lambertz; CA Wells; E Ishikawa; SK Butcher; TC Barnett; MJ Walker; A Imamura; H Ishida; T Ikebe; T Miyamoto; M Ato; S Ohga; B Lepenies; NM Van Sorge; S Yamasaki

Journal article

Lipoteichoic acid anchor triggers Mincle to drive protective immunity against invasive group A Streptococcus infection

T Imai, T Matsumura, S Mayer-Lambertz, CA Wells, E Ishikawa, SK Butcher, TC Barnett, MJ Walker, A Imamura, H Ishida, T Ikebe, T Miyamoto, M Ato, S Ohga, B Lepenies, NM Van Sorge, S Yamasaki

Proceedings of the National Academy of Sciences of the United States of America | NATL ACAD SCIENCES | Published : 2018

DOI: 10.1073/pnas.1809100115

Abstract

Group A Streptococcus (GAS) is a Gram-positive bacterial pathogen that causes a range of diseases, including fatal invasive infections. However, the mechanisms by which the innate immune system recognizes GAS are not well understood. We herein report that the C-type lectin receptor macrophage inducible C-type lectin (Mincle) recognizes GAS and initiates antibacterial immunity. Gene expression analysis of myeloid cells upon GAS stimulation revealed the contribution of the caspase recruitment domain-containing protein 9 (CARD9) pathway to the antibacterial responses. Among receptors signaling through CARD9, Mincle induced the production of inflammatory cytokines, inducible nitric oxide synthas..

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University of Melbourne Researchers

Christine Wells Author

Suzy Butcher Author

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Grants

Awarded by Takeda Science Foundation

Funding Acknowledgements

We thank T. Hara for supervision; M. Kurata, S. Iwai, X. Lu, and K. Motomura for technical support; M. Tanaka, Y. Baba, K. Kaseda, and M. Ikawa for embryonic engineering; and the Cooperative Research Project Program of the Medical Institute of Bioregulation, Kyushu University. This research was supported by Japan Society for the Promotion of Science (JSPS) KAKENHI Grants JP26293099 (to S.Y.), JP26110009 (to S.Y.), and JP16K09952 (to T. Matsumura); Japan Agency for Medical Research and Development (AMED) under Grants JP17gm0910010 (to S.Y.), JP17ak0101070 (to S.Y.), JP18fk0108075 (to S.Y.), and JP18fk0108044 (to T. Ikebe and T. Matsumura); Vidi Grant 91713303 from the Netherlands Organization for Scientific Research (to N.M.v.S.); National Health and Medical Research Council (NHMRC) Grants APP1041294 and APP1057846 (to M.J.W. and C.A.W.); and the Australian Research Council Grant SRI110001002 (to C.A.W.). S.Y. acknowledges funding from Takeda Science Foundation. B.L. acknowledges funding from the Niedersachsen-Research Network on Neuroinfectiology.