Please use this identifier to cite or link to this item: https://doi.org/10.1038/ncomms4866
Title: Parallel T-cell cloning and deep sequencing of human MAIT cells reveal stable oligoclonal TCRβ 2 repertoire
Authors: Lepore, M.
Kalinicenko, A.
Colone, A.
Paleja, B.
Singhal, A.
Tschumi, A.
Lee, B.
Poidinger, M.
Zolezzi, F.
Quagliata, L.
Sander, P.
Newell, E.
Bertoletti, A. 
Terracciano, L.
De Libero, G.
Mori, L.
Issue Date: 15-May-2014
Citation: Lepore, M., Kalinicenko, A., Colone, A., Paleja, B., Singhal, A., Tschumi, A., Lee, B., Poidinger, M., Zolezzi, F., Quagliata, L., Sander, P., Newell, E., Bertoletti, A., Terracciano, L., De Libero, G., Mori, L. (2014-05-15). Parallel T-cell cloning and deep sequencing of human MAIT cells reveal stable oligoclonal TCRβ 2 repertoire. Nature Communications 5 : -. ScholarBank@NUS Repository. https://doi.org/10.1038/ncomms4866
Abstract: Mucosal-associated invariant T (MAIT) cells are abundant in humans and recognize conserved bacterial antigens derived from riboflavin precursors, presented by the non-polymorphic MHC class I-like molecule MR1. Here we show that human MAIT cells are remarkably oligoclonal in both the blood and liver, display high inter-individual homology and exhibit a restricted length CDR3β 2 domain of the TCRVβ 2 chain. We extend this analysis to a second sub-population of MAIT cells expressing a semi-invariant TCR conserved between individuals. Similar to €̃ conventional € MAIT cells, these lymphocytes react to riboflavin-synthesizing microbes in an MR1-restricted manner and infiltrate solid tissues. Both MAIT cell types release Th0, Th1 and Th2 cytokines, and sCD40L in response to bacterial infection, show cytotoxic capacity against infected cells and promote killing of intracellular bacteria, thus suggesting important protective and immunoregulatory functions of these lymphocytes. © 2014 Macmillan Publishers Limited. All rights reserved.
Source Title: Nature Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/126834
ISSN: 20411723
DOI: 10.1038/ncomms4866
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