Journal article

CD36 family members are TCR-independent ligands for CD1 antigen-presenting molecules.

Nicholas A Gherardin, Samuel J Redmond, Hamish EG McWilliam, Catarina F Almeida, Katherine HA Gourley, Rebecca Seneviratna, Shihan Li, Robert De Rose, Fiona J Ross, Catriona V Nguyen-Robertson, Shian Su, Matthew E Ritchie, Jose A Villadangos, D Branch Moody, Daniel G Pellicci, Adam P Uldrich, Dale I Godfrey

Science Immunology | American Association for the Advancement of Science | Published : 2021

Abstract

CD1c presents lipid-based antigens to CD1c-restricted T cells, which are thought to be a major component of the human T cell pool. However, the study of CD1c-restricted T cells is hampered by the presence of an abundantly expressed, non-T cell receptor (TCR) ligand for CD1c on blood cells, confounding analysis of TCR-mediated CD1c tetramer staining. Here, we identified the CD36 family (CD36, SR-B1, and LIMP-2) as ligands for CD1c, CD1b, and CD1d proteins and showed that CD36 is the receptor responsible for non-TCR-mediated CD1c tetramer staining of blood cells. Moreover, CD36 blockade clarified tetramer-based identification of CD1c-restricted T cells and improved identification of CD1b- and ..

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Grants

Awarded by Australian Research Council (ARC)


Awarded by National Health and Medical Research Council, Australia (NHMRC)


Awarded by National Institutes of Health, USA (NIH)


Awarded by NHMRC Senior Principal Research Fellowship


Awarded by ARC


Awarded by NHMRC Senior Research Fellowship


Funding Acknowledgements

This work was supported by the Australian Research Council (ARC; CE140100011 and DP120102471), the National Health and Medical Research Council, Australia (NHMRC; 1113293 and 1145373), and the National Institutes of Health, USA (NIH; R01 AR048632). D.I.G. was supported by an NHMRC Senior Principal Research Fellowship (1117766), N.A.G. and H.E.G.M. were supported by ARC Discovery Early Career Researcher Awards (DECRA; DE210100705 and DE170100575, respectively), D.G.P. was supported by a CSL centenary fellowship, and J. A.V. was supported by an NHMRC Senior Research Fellowship (1058193). Author contributions: N.A.G. performed experiments and/or directed the experimental work. S.J.R., C.F.A., K.H.A.G., R.S., R.D.R., F.J.R., C.V.N.-R., D.B.M., D.G.P., and A.P.U. performed or assisted with cellular experiments. H.E.G.M., S.L., and J.A.V. assisted with CRISPR experiments, and S.S. and M.E.R. performed CRISPR screen data analysis. N.A.G. and D.I.G. conceived the study, cowrote the paper, and contributed equally to this work.