CD1b presents self and Borrelia burgdorferi diacylglycerols to human T cells

P Reinink; MNT Souter; TY Cheng; T van Gorkom; S Lenz; J Kubler-Kielb; K Strle; K Kremer; SFT Thijsen; AC Steere; DI Godfrey; DG Pellicci; DB Moody; I Van Rhijn

Journal article

CD1b presents self and Borrelia burgdorferi diacylglycerols to human T cells

P Reinink, MNT Souter, TY Cheng, T van Gorkom, S Lenz, J Kubler-Kielb, K Strle, K Kremer, SFT Thijsen, AC Steere, DI Godfrey, DG Pellicci, DB Moody, I Van Rhijn

European Journal of Immunology | WILEY | Published : 2019

DOI: 10.1002/eji.201847949

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Abstract

Lyme disease is a common multisystem disease caused by infection with a tick-transmitted spirochete, Borrelia burgdorferi and related Borrelia species. The monoglycosylated diacylglycerol known as B. burgdorferi glycolipid II (BbGL-II) is a major target of antibodies in sera from infected individuals. Here, we show that CD1b presents BbGL-II to human T cells and that the TCR mediates the recognition. However, we did not detect increased frequency of CD1b-BbGL-II binding T cells in the peripheral blood of Lyme disease patients compared to controls. Unexpectedly, mapping the T cell specificity for BbGL-II-like molecules using tetramers and activation assays revealed a concomitant response to C..

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University of Melbourne Researchers

Michael Souter Author

Dale Godfrey Author

Daniel Pellicci Author

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Awarded by Boehringer Ingelheim Fonds

Funding Acknowledgements

This work was supported by funding from Nederlands Wetenschappelijk Onderzoek grant 824.02.002 and the NIH (AI116604, AI04393). P.R. was supported by a Boehringer Ingelheim Fonds travel grant. M.N.T.S. was supported by an Australian Postgraduate Award. M.J.S., D.I.G., and D.G.P. are supported by the National Health and Medical Research Council (NHMRC, 1063587) and the Australian Research Council (ARC; CE140100011). D.I.G. is also supported by NHMRC Senior Principal Research Fellowship (1020770) and D.G.P. is supported by an NHMRC Career Development Fellowship (APP1144308).