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NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells.

J Exp Med. 2020 Aug 03;217(8)
Marina Babic 1 , Christoforos Dimitropoulos 2 , Quirin Hammer 2 , Christina Stehle 2 , Frederik Heinrich 3 , Assel Sarsenbayeva 2 , Almut Eisele 2 , Pawel Durek 4 , Mir-Farzin Mashreghi 3 , Berislav Lisnic 5 , Jacques Van Snick 6 , Max Löhning 7 , Simon Fillatreau 8 , David R Withers 9 , Nicola Gagliani 10 , Samuel Huber 10 , Richard A Flavell 11 , Bojan Polic 5 , Chiara Romagnani 1
Marina Babic 1 , Christoforos Dimitropoulos 2 , Quirin Hammer 2 , Christina Stehle 2 , Frederik Heinrich 3 , Assel Sarsenbayeva 2 , Almut Eisele 2 , Pawel Durek 4 , Mir-Farzin Mashreghi 3 , Berislav Lisnic 5 , Jacques Van Snick 6 , Max Löhning 7 , Simon Fillatreau 8 , David R Withers 9 , Nicola Gagliani 10 , Samuel Huber 10 , Richard A Flavell 11 , Bojan Polic 5 , Chiara Romagnani 1
+ et al

[No authors listed]

Author information
  • 1 Division of Gastroenterology, Infectiology and Rheumatology, Medical Department I, Charité-Universitätsmedizin Berlin, Berlin, Germany.
  • 2 Innate Immunity, German Rheumatism Research Centre-a Leibniz Institute, Berlin, Germany.
  • 3 Therapeutic Gene Regulation, German Rheumatism Research Centre-a Leibniz Institute, Berlin, Germany.
  • 4 Cell Biology, German Rheumatism Research Centre-a Leibniz Institute, Berlin, Germany.
  • 5 Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Croatia.
  • 6 Ludwig Institute for Cancer Research, Brussels, Belgium.
  • 7 Experimental Immunology and Osteoarthritis Research, Department of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
  • 8 Institut Necker-Enfants Malades, INSERM U1151/CNRS UMR8253, Faculté de Médecine Paris Descartes, Paris, France.
  • 9 Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
  • 10 Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
  • 11 Howard Hughes Medical Institute, Yale University, New Haven, CT.

摘要


NKG2D is a danger sensor expressed on different subsets of innate and adaptive lymphocytes. Despite its established role as a potent activator of the immune system, NKG2D-driven regulation of CD4+ T helper (Th) cell-mediated immunity remains unclear. In this study, we demonstrate that NKG2D modulates Th1 and proinflammatory T-bet+ Th17 cell effector functions in vitro and in vivo. In particular, NKG2D promotes higher production of proinflammatory cytokines by Th1 and T-bet+ Th17 cells and reinforces their transcription of type 1 signature genes, including Tbx21. Conditional deletion of NKG2D in T cells impairs the ability of antigen-specific CD4+ T cells to promote inflammation in vivo during antigen-induced arthritis and experimental autoimmune encephalomyelitis, indicating that NKG2D is an important target for the amelioration of Th1- and Th17-mediated chronic inflammatory diseases.