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    Glutamic acid decarboxylase 67-reactive T cells: a marker of insulin-dependent diabetes.

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    Author
    Honeyman, MC; Cram, DS; Harrison, LC
    Date
    1993-02-01
    Source Title
    Journal of Experimental Medicine
    Publisher
    Rockefeller University Press
    University of Melbourne Author/s
    Harrison, Leonard
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Honeyman, M. C., Cram, D. S. & Harrison, L. C. (1993). Glutamic acid decarboxylase 67-reactive T cells: a marker of insulin-dependent diabetes.. J Exp Med, 177 (2), pp.535-540. https://doi.org/10.1084/jem.177.2.535.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259241
    DOI
    10.1084/jem.177.2.535
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190899
    Abstract
    Glutamic acid decarboxylase (GAD) has been shown to be a target of autoantibodies in insulin-dependent diabetes (IDD). Two forms of GAD, with molecular weights of 67,000 and 65,000, have been cloned from separate genes. As pancreatic islet beta cell destruction DD is an autoimmune process mediated by T cells, we sought to determine if recombinant GAD67 was recognized by T cells in IDD subjects and particularly their first-degree relatives with islet cell antibodies known to be at risk for IDD. The central regions of human islet and brain GAD67 (amino acids 208-404) were cloned as fusion proteins with glutathione-S-transferase (GST). Proliferation of peripheral blood T cells in the presence of recombinant GAD67 was significantly higher in both at-risk relatives and recent-onset IDD subjects than in other autoimmune disease subjects and human histocompatibility leukocyte antigen (HLA)-matched healthy controls. Thus, 12 of 29 (41%) at-risk relatives and 11 of 29 (38%) recent-onset IDD subjects responded to GAD67, compared with 1 of 7 (14%) other autoimmune disease subjects and 1 of 23 (4%) HLA-matched controls. T cell responses to GST alone or to tetanus toxoid were not different between the groups. These findings demonstrate that GAD67 is a target autoantigen of T cells in IDD and suggest the possibility that GAD-reactive T cells may delineate asymptomatic subjects at increased risk for IDD.

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