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T-Cell Responsiveness to an Oncogenic Peripheral Protein and Spontaneous Autoimmunity in Transgenic Mice

Terrence Geiger, Linda R. Gooding and Richard A. Flavell
Proceedings of the National Academy of Sciences of the United States of America
Vol. 89, No. 7 (Apr. 1, 1992), pp. 2985-2989
Stable URL: http://www.jstor.org/stable/2359018
Page Count: 5
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
T-Cell Responsiveness to an Oncogenic Peripheral Protein and Spontaneous Autoimmunity in Transgenic Mice
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Abstract

Why T cells develop autoimmune reactivity to some antigens and tolerance to others is unknown. Various mechanisms can provide for T-cell tolerance. These include deletion in the thymus, exhaustive differentiation in the periphery, T-cell receptor and coreceptor downregulation, and anergy. Which mechanisms normally provide for tolerance to antigens expressed on specific tissues and why they sometimes fail is unclear. To understand this, we analyzed how a tissue-specific protein with defined timing and location of expression is recognized by T cells so as to induce tolerance or autoimmunity. We crossed mice expressing the simian virus 40 large tumor antigen on pancreatic acini beginning 4-25 days after birth with mice transgenic for a rearranged T-cell receptor that recognizes this antigen presented by the class I major histocompatibility complex molecule H-2Kk. No T-cell tolerance was found; rather, T-cell reactivity accompanied lymphocytic infiltration and pancreatic acinar destruction. This result argues that T cells may become spontaneously autoreactive to certain postnatally expressed peripheral proteins and that this reactivity may lead to autoimmune disease.

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