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Antigen presenting function of class II MHC expressing pancreatic beta cells

Nature volume 336, pages 476–479 (1988)Cite this article

Abstract

Class II major histocompatibility complex (MHC) gene expression in the mouse is generally limited to thymic epithelium and bone marrow-derived cells such as B lymphocytes and cells of the macrophage/dendritic cell lineage (MØ/DC). Class II-bearing B lymphocytes and MØ/DC possess antigen presenting cell (APC) function; that is, they can stimulate T lymphocytes reactive to either antigen plus MHC or foreign MHC alone. To assess whether non-bone-marrow-derived cells can acquire APC function and elicit graft rejection through expression of class II, we studied transgenic pancreatic islet beta cells that express a foreign class II (I-E) molecule. In vivo, grafts of I-E+ transgenic islets into I-E- naive hosts are not rejected unless the host is primed by an injection of I-E+ spleen cells. In vitro, the I-E+ beta cells are unable to stimulate T lymphocytes reactive to I-E plus a peptide antigen. Paradoxically, they induce antigen specific unresponsiveness in the T cells. We propose that expression of class II on non-lymphoid cells may serve as an extrathymic mechanism for maintaining self tolerance.

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Authors and Affiliations

  1. Department of Surgery, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, 19104, USA

    James Markmann & Ali Naji

  2. Laboratory of Reproductive Physiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, 19104, USA

    David Lo & Ralph L. Brinster

  3. Howard Hughes Medical Institute, Department of Biochemistry, University of Washington, Seattle, Washington, 98195, USA

    Richard D. Palmiter

  4. Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania, 19104, USA

    Ellen Heber-Katz

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  1. James Markmann
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  6. Ellen Heber-Katz
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Markmann, J., Lo, D., Naji, A. et al. Antigen presenting function of class II MHC expressing pancreatic beta cells. Nature 336, 476–479 (1988). https://doi.org/10.1038/336476a0

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