CD1b-restricted GEM T cell responses are modulated by Mycobacterium tuberculosis mycolic acid meromycolate chains

Andrew Chancellor, Anna S. Tocheva, Chris Cave-Ayland, Liku Tezera, Andrew White, Juma'a R. Al Dulayymi, John S. Bridgeman, Ivo Tews, Susan Wilson, Nikolai M. Lissin, Marc Tebruegge, Ben Marshall, Sally Sharpe, Tim Elliott, Chris Kriton Skylaris, Jonathan W. Essex, Mark S. Baird, Stephan Gadola, Paul Elkington, Salah Mansour

Research output: Contribution to journalArticlepeer-review

37 Scopus citations

Abstract

Tuberculosis (TB), caused by Mycobacterium tuberculosis, remains a major human pandemic. Germline-encoded mycolyl lipid-reactive (GEM) T cells are donor-unrestricted and recognize CD1b-presented mycobacterial mycolates. However, the molecular requirements governing mycolate antigenicity for the GEM T cell receptor (TCR) remain poorly understood. Here, we demonstrate CD1b expression in TB granulomas and reveal a central role for meromycolate chains in influencing GEM-TCR activity. Meromycolate fine structure influences T cell responses in TB-exposed individuals, and meromycolate alterations modulate functional responses by GEM-TCRs. Computational simulations suggest that meromycolate chain dynamics regulate mycolate head group movement, thereby modulating GEM-TCR activity. Our findings have significant implications for the design of future vaccines that target GEM T cells.

Original languageEnglish
Pages (from-to)E10956-E10964
JournalProceedings of the National Academy of Sciences of the United States of America
Volume114
Issue number51
DOIs
StatePublished - 19 Dec 2017
Externally publishedYes

Keywords

  • CD1b
  • GEM T cells
  • Molecular dynamics
  • Mycobacterium tuberculosis
  • Mycolate lipids

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