Antigen-loaded MR1 tetramers define T cell receptor heterogeneity in mucosal-associated invariant T cells

R Reantragoon; AJ Corbett; IG Sakala; NA Gherardin; JB Furness; Z Chen; SBG Eckle; AP Uldrich; RW Birkinshaw; O Patel; L Kostenko; B Meehan; K Kedzierska; L Liu; DP Fairlie; TH Hansen; DI Godfrey; J Rossjohn; J McCluskey; L Kjer-Nielsen

Journal article

Antigen-loaded MR1 tetramers define T cell receptor heterogeneity in mucosal-associated invariant T cells

R Reantragoon, AJ Corbett, IG Sakala, NA Gherardin, JB Furness, Z Chen, SBG Eckle, AP Uldrich, RW Birkinshaw, O Patel, L Kostenko, B Meehan, K Kedzierska, L Liu, DP Fairlie, TH Hansen, DI Godfrey, J Rossjohn, J McCluskey, L Kjer-Nielsen

Journal of Experimental Medicine | ROCKEFELLER UNIV PRESS | Published : 2013

DOI: 10.1084/jem.20130958

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Abstract

Mucosal-associated invariant T cells (MAIT cells) express a semi-invariant T cell receptor (TCR) α-chain, TRAV1-2-TRAJ33, and are activated by vitamin B metabolites bound by the major histocompatibility complex (MHC)-related class I-like molecule, MR1. Understanding MAIT cell biology has been restrained by the lack of reagents to specifically identify and characterize these cells. Furthermore, the use of surrogate markers may misrepresent the MAIT cell population. We show that modified human MR1 tetramers loaded with the potent MAIT cell ligand, reduced 6-hydroxymethyl-8-d-ribityllumazine (rRL-6-CH2OH), specifically detect all human MAIT cells. Tetramer+MAIT subsets were predominantly CD8+or..

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University of Melbourne Researchers

Alexandra Corbett Author

Nicholas Gherardin Author

John Furness Author

Zhenjun Chen Author

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Awarded by National Institute of Allergy and Infectious Diseases

Funding Acknowledgements

This research was supported by the National Health and Medical Research Council of Australia (NHMRC). T. H. Hansen was supported by National Institutes of Health grant AI046553. R. Reantragoon was supported by the Faculty of Medicine, Chulalongkorn University and Chulalongkorn Hospital, Thai Red Cross Society scholarships. N.A. Gherardin was supported by a Leukemia Foundation postgraduate scholarship. D. P. Fairlie and D. I. Godfrey were supported by NHMRC Senior Principal Research Fellowships. O. Patel was supported by an Australian Research Council Future Fellowship. J. Rossjohn was supported by an NHMRC Australia Fellowship.