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10.4049/jimmunol.1700406

http://scihub22266oqcxt.onion/10.4049/jimmunol.1700406
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C5501482!5501482!28539428
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suck abstract from ncbi


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pmid28539428      J+Immunol 2017 ; 199 (1): 33-8
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  • Dual TCR? expression poses an autoimmune hazard by limiting Treg 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): 33-8 PMID28539428show 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 (T1D). 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 (Treg) cell commitment, resulting in a more tolerogenic Treg to conventional T (Tconv) 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 Treg cell lineage.
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