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Jarid2 is induced by TCR signalling and controls iNKT cell maturation

Author

Listed:
  • Renata M. Pereira

    (La Jolla Institute for Allergy and Immunology)

  • Gustavo J. Martinez

    (La Jolla Institute for Allergy and Immunology
    Present address: Genomics Core, The Scripps Research Institute, Jupiter, FL 33458, USA)

  • Isaac Engel

    (La Jolla Institute for Allergy and Immunology)

  • Fernando Cruz-Guilloty

    (Bascom Palmer Eye Institute, University of Miami Miller School of Medicine
    Present address: Immucor, Inc., Norcross, Georgia 30091, USA)

  • Bianca A. Barboza

    (La Jolla Institute for Allergy and Immunology
    Present address: Division of Cellular Biology, Brazilian National Cancer Institute (INCA), Rio de Janeiro 20230-130, Brazil)

  • Ageliki Tsagaratou

    (La Jolla Institute for Allergy and Immunology)

  • Chan-Wang J. Lio

    (La Jolla Institute for Allergy and Immunology)

  • Leslie J. Berg

    (University of Massachusetts Medical School)

  • Youngsook Lee

    (School of Medicine and Public Health, University of Wisconsin)

  • Mitchell Kronenberg

    (La Jolla Institute for Allergy and Immunology)

  • Hozefa S. Bandukwala

    (La Jolla Institute for Allergy and Immunology
    Present address: Pfizer Inc, Cambridge, Massachusetts 02139, USA)

  • Anjana Rao

    (La Jolla Institute for Allergy and Immunology
    University of California at San Diego)

Abstract

Jarid2 is a reported component of three lysine methyltransferase complexes, polycomb repressive complex 2 (PRC2) that methylates histone 3 lysine 27 (H3K27), and GLP-G9a and SETDB1 complexes that methylate H3K9. Here we show that Jarid2 is upregulated upon TCR stimulation and during positive selection in the thymus. Mice lacking Jarid2 in T cells display an increase in the frequency of IL-4-producing promyelocytic leukemia zinc finger (PLZF)hi immature invariant natural killer T (iNKT) cells and innate-like CD8+ cells; Itk-deficient mice, which have a similar increase of innate-like CD8+ cells, show blunted upregulation of Jarid2 during positive selection. Jarid2 binds to the Zbtb16 locus, which encodes PLZF, and thymocytes lacking Jarid2 show increased PLZF and decreased H3K9me3 levels. Jarid2-deficient iNKT cells perturb Th17 differentiation, leading to reduced Th17-driven autoimmune pathology. Our results establish Jarid2 as a novel player in iNKT cell maturation that regulates PLZF expression by modulating H3K9 methylation.

Suggested Citation

  • Renata M. Pereira & Gustavo J. Martinez & Isaac Engel & Fernando Cruz-Guilloty & Bianca A. Barboza & Ageliki Tsagaratou & Chan-Wang J. Lio & Leslie J. Berg & Youngsook Lee & Mitchell Kronenberg & Hoze, 2014. "Jarid2 is induced by TCR signalling and controls iNKT cell maturation," Nature Communications, Nature, vol. 5(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5540
    DOI: 10.1038/ncomms5540
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