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10.1016/j.immuni.2017.06.021

http://scihub22266oqcxt.onion/10.1016/j.immuni.2017.06.021
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28723546!ä!28723546

suck abstract from ncbi


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pmid28723546      Immunity 2017 ; 47 (1): 135-147.e5
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  • Local Modulation of Antigen-Presenting Cell Development after Resolution of Pneumonia Induces Long-Term Susceptibility to Secondary Infections #MMPMID28723546
  • Roquilly A; McWilliam HEG; Jacqueline C; Tian Z; Cinotti R; Rimbert M; Wakim L; Caminschi I; Lahoud MH; Belz GT; Kallies A; Mintern JD; Asehnoune K; Villadangos JA
  • Immunity 2017[Jul]; 47 (1): 135-147.e5 PMID28723546show ga
  • Lung infections cause prolonged immune alterations and elevated susceptibility to secondary pneumonia. We found that, after resolution of primary viral or bacterial pneumonia, dendritic cells (DC), and macrophages exhibited poor antigen-presentation capacity and secretion of immunogenic cytokines. Development of these "paralyzed" DCs and macrophages depended on the immunosuppressive microenvironment established upon resolution of primary infection, which involved regulatory T (Treg) cells and the cytokine TGF-beta. Paralyzed DCs secreted TGF-beta and induced local Treg cell accumulation. They also expressed lower amounts of IRF4, a transcription factor associated with increased antigen-presentation capacity, and higher amounts of Blimp1, a transcription factor associated with tolerogenic functions, than DCs present during primary infection. Blimp1 expression in DC of humans suffering sepsis or trauma correlated with severity and complicated outcomes. Our findings describe mechanisms underlying sepsis- and trauma-induced immunosuppression, reveal prognostic markers of susceptibility to secondary infections and identify potential targets for therapeutic intervention.
  • |Aged[MESH]
  • |Animals[MESH]
  • |Antigen Presentation[MESH]
  • |Cell Differentiation[MESH]
  • |Cells, Cultured[MESH]
  • |Dendritic Cells/*immunology[MESH]
  • |Escherichia coli[MESH]
  • |Escherichia coli Infections/*immunology[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Immune Tolerance[MESH]
  • |Influenza A virus/*immunology[MESH]
  • |Interferon Regulatory Factors/genetics/metabolism[MESH]
  • |Macrophages/*immunology[MESH]
  • |Male[MESH]
  • |Mice[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Mice, Knockout[MESH]
  • |Middle Aged[MESH]
  • |Orthomyxoviridae Infections/*immunology[MESH]
  • |Pneumonia/*immunology[MESH]
  • |Positive Regulatory Domain I-Binding Factor 1[MESH]
  • |Sepsis/*immunology[MESH]
  • |T-Lymphocytes, Regulatory/immunology[MESH]
  • |Transcription Factors/genetics/metabolism[MESH]


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