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The mouse NKR-P1B:Clr-b recognition system is a negative regulator of innate immune responses.

Blood. 2015 Apr 02;125(14):2217-27. Epub 2015 Jan 22
Mir Munir A Rahim 1 , Peter Chen 2 , Amelia N Mottashed 1 , Ahmad Bakur Mahmoud 3 , Midhun J Thomas 1 , Qinzhang Zhu 4 , Colin G Brooks 5 , Vicky Kartsogiannis 6 , Matthew T Gillespie 7 , James R Carlyle 2 , Andrew P Makrigiannis 1
Mir Munir A Rahim 1 , Peter Chen 2 , Amelia N Mottashed 1 , Ahmad Bakur Mahmoud 3 , Midhun J Thomas 1 , Qinzhang Zhu 4 , Colin G Brooks 5 , Vicky Kartsogiannis 6 , Matthew T Gillespie 7 , James R Carlyle 2 , Andrew P Makrigiannis 1
+ et al

[No authors listed]

Author information
  • 1 Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada;
  • 2 Department of Immunology, University of Toronto, Sunnybrook Research Institute, Toronto, ON, Canada;
  • 3 Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada; College of Applied Medical Sciences, Taibah University, Madinah Munawwarah, Kingdom of Saudi Arabia;
  • 4 Transgenic Core Facility, Clinical Research Institute of Montreal, Montreal, QC, Canada;
  • 5 Institute of Cell and Molecular Biosciences, The Medical School, Newcastle, United Kingdom;
  • 6 Prince Henry's Institute, Monash Medical Centre, Clayton, VIC, Australia; and.
  • 7 Prince Henry's Institute, Monash Medical Centre, Clayton, VIC, Australia; and Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC, Australia.

摘要

NKR-P1B is a homodimeric type II transmembrane C-type lectinlike receptor that inhibits natural killer (NK) cell function upon interaction with its cognate C-type lectin-related ligand, Clr-b. The NKR-P1B:Clr-b interaction represents a major histocompatibility complex class I (MHC-I)-independent missing-self recognition system that monitors cellular Clr-b levels. We have generated NKR-P1B(B6)-deficient (Nkrp1b(-/-)) mice to study the role of NKR-P1B in NK cell development and function in vivo. NK cell inhibition by Clr-b is abolished in Nkrp1b(-/-) mice, confirming the inhibitory nature of NKR-P1B(B6). Inhibitory receptors also promote NK cell tolerance and responsiveness to stimulation; hence, NK cells expressing NKR-P1B(B6) and Ly49C/I display augmented responsiveness to activating signals vs NK cells expressing either or none of the receptors. In addition, Nkrp1b(-/-) mice are defective in rejecting cells lacking Clr-b, supporting a role for NKR-P1B(B6) in MHC-I-independent missing-self recognition of Clr-b in vivo. In contrast, MHC-I-dependent missing-self recognition is preserved in Nkrp1b(-/-) mice. Interestingly, spontaneous myc-induced B lymphoma cells may selectively use NKR-P1B:Clr-b interactions to escape immune surveillance by wild-type, but not Nkrp1b(-/-), NK cells. These data provide direct genetic evidence of a role for NKR-P1B in NK cell tolerance and MHC-I-independent missing-self recognition.

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