TCR signal strength controls thymic differentiation of iNKT cell subsets View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Kathryn D. Tuttle, S. Harsha Krovi, Jingjing Zhang, Romain Bedel, Laura Harmacek, Lisa K. Peterson, Leonard L. Dragone, Adam Lefferts, Catherine Halluszczak, Kent Riemondy, Jay R. Hesselberth, Anjana Rao, Brian P. O’Connor, Philippa Marrack, James Scott-Browne, Laurent Gapin

ABSTRACT

During development in the thymus, invariant natural killer T (iNKT) cells commit to one of three major functionally different subsets, iNKT1, iNKT2, and iNKT17. Here, we show that T cell antigen receptor (TCR) signal strength governs the development of iNKT cell subsets, with strong signaling promoting iNKT2 and iNKT17 development. Altering TCR diversity or signaling diminishes iNKT2 and iNKT17 cell subset development in a cell-intrinsic manner. Decreased TCR signaling affects the persistence of Egr2 expression and the upregulation of PLZF. By genome-wide comparison of chromatin accessibility, we identify a subset of iNKT2-specific regulatory elements containing NFAT and Egr binding motifs that is less accessible in iNKT2 cells that develop from reduced TCR signaling. These data suggest that variable TCR signaling modulates regulatory element activity at NFAT and Egr binding sites exerting a determinative influence on the dynamics of gene enhancer accessibility and the developmental fate of iNKT cells. More... »

PAGES

2650

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-018-05026-6

    DOI

    http://dx.doi.org/10.1038/s41467-018-05026-6

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1105348570

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/29985393


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