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    Initiation of autoimmune diabetes by developmentally regulated presentation of islet cell antigens in the pancreatic lymph nodes

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    339
    Author
    Hoglund, P; Mintern, J; Waltzinger, C; Heath, W; Benoist, C; Mathis, D
    Date
    1999-01-18
    Source Title
    Journal of Experimental Medicine
    Publisher
    ROCKEFELLER UNIV PRESS
    University of Melbourne Author/s
    Mintern, Justine; Heath, William
    Affiliation
    Microbiology and Immunology
    Biochemistry and Molecular Biology
    Metadata
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    Document Type
    Journal Article
    Citations
    Hoglund, P., Mintern, J., Waltzinger, C., Heath, W., Benoist, C. & Mathis, D. (1999). Initiation of autoimmune diabetes by developmentally regulated presentation of islet cell antigens in the pancreatic lymph nodes. JOURNAL OF EXPERIMENTAL MEDICINE, 189 (2), pp.331-339. https://doi.org/10.1084/jem.189.2.331.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/260408
    DOI
    10.1084/jem.189.2.331
    Abstract
    Little is known about the events triggering lymphocyte invasion of the pancreatic islets in prelude to autoimmune diabetes. For example, where islet-reactive T cells first encounter antigen has not been identified. We addressed this issue using BDC2.5 T cell receptor transgenic mice, which express a receptor recognizing a natural islet beta cell antigen. In BDC2.5 animals, activated T cells were found only in the islets and the lymph nodes draining them, and there was a close temporal correlation between lymph node T cell activation and islet infiltration. When naive BDC2.5 T cells were transferred into nontransgenic recipients, proliferating cells were observed only in pancreatic lymph nodes, and this occurred significantly before insulitis was detectable. Surprisingly, proliferation was not seen in 10-day-old recipients. This age-dependent dichotomy was reproduced in a second transfer system based on an unrelated antigen artificially expressed on beta cells. We conclude that beta cell antigens are transported specifically to pancreatic lymph nodes, where they trigger reactive T cells to invade the islets. Systemic or extrapancreatic T cell priming, indicative of activation via molecular mimicry or superantigens, was not seen. Compromised presentation of beta cell antigens in the pancreatic lymph nodes of juvenile animals may be the root of a first "checkpoint" in diabetes progression.

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