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γδ T cells control humoral immune response by inducing T follicular helper cell differentiation

Author

Listed:
  • Rafael M. Rezende

    (Harvard Medical School)

  • Amanda J. Lanser

    (Harvard Medical School)

  • Stephen Rubino

    (Harvard Medical School)

  • Chantal Kuhn

    (Harvard Medical School)

  • Nathaniel Skillin

    (Harvard Medical School)

  • Thais G. Moreira

    (Harvard Medical School)

  • Shirong Liu

    (Harvard Medical School)

  • Galina Gabriely

    (Harvard Medical School)

  • Bruna A. David

    (Federal University of Minas Gerais)

  • Gustavo B. Menezes

    (Federal University of Minas Gerais)

  • Howard L. Weiner

    (Harvard Medical School)

Abstract

γδ T cells have many known functions, including the regulation of antibody responses. However, how γδ T cells control humoral immunity remains elusive. Here we show that complete Freund’s adjuvant (CFA), but not alum, immunization induces a subpopulation of CXCR5-expressing γδ T cells in the draining lymph nodes. TCRγδ+CXCR5+ cells present antigens to, and induce CXCR5 on, CD4 T cells by releasing Wnt ligands to initiate the T follicular helper (Tfh) cell program. Accordingly, TCRδ−/− mice have impaired germinal center formation, inefficient Tfh cell differentiation, and reduced serum levels of chicken ovalbumin (OVA)-specific antibodies after CFA/OVA immunization. In a mouse model of lupus, TCRδ−/− mice develop milder glomerulonephritis, consistent with decreased serum levels of lupus-related autoantibodies, when compared with wild type mice. Thus, modulation of the γδ T cell-dependent humoral immune response may provide a novel therapy approach for the treatment of antibody-mediated autoimmunity.

Suggested Citation

  • Rafael M. Rezende & Amanda J. Lanser & Stephen Rubino & Chantal Kuhn & Nathaniel Skillin & Thais G. Moreira & Shirong Liu & Galina Gabriely & Bruna A. David & Gustavo B. Menezes & Howard L. Weiner, 2018. "γδ T cells control humoral immune response by inducing T follicular helper cell differentiation," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-05487-9
    DOI: 10.1038/s41467-018-05487-9
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