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10.1038/ni.3580

http://scihub22266oqcxt.onion/10.1038/ni.3580
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C5558830!5558830!27695001
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suck abstract from ncbi


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pmid27695001      Nat+Immunol 2016 ; 17 (12): 1373-80
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  • Identification of a role for TRIM29 in the control of innate immunity in the respiratory tract #MMPMID27695001
  • Xing J; Weng L; Yuan B; Wang Z; Jia L; Jin R; Lu H; Li XC; Liu YJ; Zhang Z
  • Nat Immunol 2016[Dec]; 17 (12): 1373-80 PMID27695001show ga
  • The respiratory tract is heavily populated with innate immune cells, but the mechanisms that control such cells are poorly defined. Here we found that the E3 ubiquitin ligase TRIM29 was a selective regulator of the activation of alveolar macrophages, the expression of type I interferons and the production of proinflammatory cytokines in the lungs. We found that deletion of TRIM29 enhanced macrophage production of type I interferons and protected mice from infection with influenza virus, while challenge of Trim29?/? mice with Haemophilus influenzae resulted in lethal lung inflammation due to massive production of proinflammatory cytokines by macrophages. Mechanistically, we demonstrated that TRIM29 inhibited interferon-regulatory factors and signaling via the transcription factor NF-?B by degrading the adaptor NEMO and that TRIM29 directly bound NEMO and subsequently induced its ubiquitination and proteolytic degradation. These data identify TRIM29 as a key negative regulator of alveolar macrophages and might have important clinical implications for local immunity and immunopathology.
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