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10.4049/jimmunol.1700406

http://scihub22266oqcxt.onion/10.4049/jimmunol.1700406
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suck abstract from ncbi


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pmid28539428
      J+Immunol 2017 ; 199 (1 ): 33-38
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  • Cutting Edge: Dual TCR? Expression Poses an Autoimmune Hazard by Limiting Regulatory T Cell Generation #MMPMID28539428
  • Schuldt NJ ; Auger JL ; Spanier JA ; Martinov T ; Breed ER ; Fife BT ; Hogquist KA ; Binstadt BA
  • J Immunol 2017[Jul]; 199 (1 ): 33-38 PMID28539428 show ga
  • Despite accounting for 10-30% of the T cell population in mice and humans, the role of dual TCR-expressing T cells in immunity remains poorly understood. It has been hypothesized that dual TCR T cells pose an autoimmune hazard by allowing self-reactive TCRs to escape thymic selection. We revisited this hypothesis using the NOD murine model of type 1 diabetes. We bred NOD mice hemizygous at both TCR? and ? (TCR?(+/-) ?(+/-)) loci, rendering them incapable of producing dual TCR T cells. We found that the lack of dual TCR? expression skewed the insulin-specific thymocyte population toward greater regulatory T (T(reg)) cell commitment, resulting in a more tolerogenic T(reg) to conventional T cell ratio and protection from diabetes. These data support a novel hypothesis by which dual TCR expression can promote autoimmunity by limiting agonist selection of self-reactive thymocytes into the T(reg) cell lineage.
  • |*Autoimmunity [MESH]
  • |Animals [MESH]
  • |Diabetes Mellitus, Type 1/immunology [MESH]
  • |Mice [MESH]
  • |Mice, Inbred NOD [MESH]
  • |Receptors, Antigen, T-Cell, alpha-beta/*genetics/*immunology [MESH]
  • |T-Lymphocytes, Regulatory/*immunology/physiology [MESH]


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