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10.4049/jimmunol.1203302

http://scihub22266oqcxt.onion/10.4049/jimmunol.1203302
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suck abstract from ncbi


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pmid23667113
      J+Immunol 2013 ; 190 (12 ): 6115-25
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  • Viral antigen induces differentiation of Foxp3+ natural regulatory T cells in influenza virus-infected mice #MMPMID23667113
  • Bedoya F ; Cheng GS ; Leibow A ; Zakhary N ; Weissler K ; Garcia V ; Aitken M ; Kropf E ; Garlick DS ; Wherry EJ ; Erikson J ; Caton AJ
  • J Immunol 2013[Jun]; 190 (12 ): 6115-25 PMID23667113 show ga
  • We examined the formation, participation, and functional specialization of virus-reactive Foxp3(+) regulatory T cells (Tregs) in a mouse model of influenza virus infection. "Natural" Tregs generated intrathymically, based on interactions with a self-peptide, proliferated in response to a homologous viral Ag in the lungs and, to a lesser extent, in the lung-draining mediastinal lymph nodes (medLNs) of virus-infected mice. In contrast, conventional CD4(+) T cells with identical TCR specificity underwent little or no conversion to become "adaptive" Tregs. The virus-reactive Tregs in the medLNs and the lungs of infected mice upregulated a variety of molecules associated with Treg activation, as well as acquired expression of molecules (T-bet, Blimp-1, and IL-10) that confer functional specialization to Tregs. Notably, however, the phenotypes of the T-bet(+) Tregs obtained from these sites were distinct, because Tregs isolated from the lungs expressed significantly higher levels of T-bet, Blimp-1, and IL-10 than did Tregs from the medLNs. Adoptive transfer of Ag-reactive Tregs led to decreased proliferation of antiviral CD4(+) and CD8(+) effector T cells in the lungs of infected hosts, whereas depletion of Tregs had a reciprocal effect. These studies demonstrate that thymically generated Tregs can become activated by a pathogen-derived peptide and acquire discrete T-bet(+) Treg phenotypes while participating in and modulating an antiviral immune response.
  • |Adoptive Transfer [MESH]
  • |Animals [MESH]
  • |Antigens, Viral/immunology [MESH]
  • |Cell Differentiation/immunology [MESH]
  • |Flow Cytometry [MESH]
  • |Forkhead Transcription Factors/immunology [MESH]
  • |Lymphocyte Activation/*immunology [MESH]
  • |Mice [MESH]
  • |Mice, Inbred BALB C [MESH]
  • |Mice, Transgenic [MESH]
  • |Orthomyxoviridae Infections/*immunology [MESH]
  • |Orthomyxoviridae/immunology [MESH]
  • |Phenotype [MESH]
  • |Real-Time Polymerase Chain Reaction [MESH]
  • |Reverse Transcriptase Polymerase Chain Reaction [MESH]
  • |T-Lymphocyte Subsets/cytology/*immunology [MESH]


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