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Extreme Th1 bias of invariant Vα24JαQ T cells in type 1 diabetes

Author

Listed:
  • S. Brian Wilson

    (Harvard University)

  • Sally C. Kent

    (Center for Neurologic Diseases, Brigham and Women's Hospital, Brigham and Women's Hospital Harvard Medical School)

  • Kurt T. Patton

    (Center for Neurologic Diseases, Brigham and Women's Hospital, Brigham and Women's Hospital Harvard Medical School)

  • Tihamer Orban

    (Immunology Section, Joslin Diabetes Center, Brigham and Women's Hospital Harvard Medical School)

  • Richard A. Jackson

    (Immunology Section, Joslin Diabetes Center, Brigham and Women's Hospital Harvard Medical School)

  • Mark Exley

    (Cancer Biology Program, Beth Israel Deaconess Medical Center, Brigham and Women's Hospital Harvard Medical School)

  • Steven Porcelli

    (Lymphocyte Biology Section, Immunology and Allergy, Brigham and Women's Hospital Harvard Medical School)

  • Desmond A. Schatz

    (University of Florida)

  • Mark A. Atkinson

    (University of Florida)

  • Steven P. Balk

    (Cancer Biology Program, Beth Israel Deaconess Medical Center, Brigham and Women's Hospital Harvard Medical School)

  • Jack L. Strominger

    (Harvard University)

  • David A. Hafler

    (Center for Neurologic Diseases, Brigham and Women's Hospital, Brigham and Women's Hospital Harvard Medical School)

Abstract

Type 1 diabetes (insulin-dependent diabetes mellitus, IDDM) is a disease controlled by the major histocompatibility complex (MHC) which results from T-cell-mediated destruction of pancreatic β-cells1. The incomplete concordance in identical twins and the presence of autoreactive T cells and autoantibodies in individuals who do not develop diabetes suggest that other abnormalities must occur in the immune system for disease to result2,3. We therefore investigated a series of at-risk non-progressors and type1 diabetic patients (including five identical twin/triplet sets discordant for disease). The diabetic siblings had lower frequencies of CD4−CD8− Vα24JαQ+ T cells compared with their non-diabetic sibling. All 56 Vα24JαQ+ clones isolated from the diabetic twins/triplets secreted only interferon (IFN)-γ upon stimulation; in contrast, 76 of 79 clones from the at-risk non-progressors and normals secreted both interleukin (IL)-4 and IFN-γ. Half of the at-risk non-progressors had high serum levels of IL-4 and IFN-γ. These results support a model for IDDM in which Th1-cell-mediated tissue damage is initially regulated by Vα24JαQ+ T cells producing both cytokines; the loss of their capacity to secrete IL-4 is correlated with IDDM.

Suggested Citation

  • S. Brian Wilson & Sally C. Kent & Kurt T. Patton & Tihamer Orban & Richard A. Jackson & Mark Exley & Steven Porcelli & Desmond A. Schatz & Mark A. Atkinson & Steven P. Balk & Jack L. Strominger & Davi, 1998. "Extreme Th1 bias of invariant Vα24JαQ T cells in type 1 diabetes," Nature, Nature, vol. 391(6663), pages 177-181, January.
    • Handle: RePEc:nat:nature:v:391:y:1998:i:6663:d:10.1038_34419
    DOI: 10.1038/34419
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