Suppression of adaptive NK cell expansion by macrophage-mediated phagocytosis inhibited by 2B4-CD48.

Autor:	Li R; Laboratory of Molecular Oncology, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC H2W 1R7, Canada; Department of Medicine, McGill University, Montréal, QC H3G 1Y6, Canada., Galindo CC; Laboratory of Molecular Oncology, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC H2W 1R7, Canada; Department of Medicine, McGill University, Montréal, QC H3G 1Y6, Canada., Davidson D; Laboratory of Molecular Oncology, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC H2W 1R7, Canada., Guo H; Laboratory of Molecular Oncology, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC H2W 1R7, Canada; Department of Medicine, McGill University, Montréal, QC H3G 1Y6, Canada., Zhong MC; Laboratory of Molecular Oncology, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC H2W 1R7, Canada., Qian J; Laboratory of Molecular Oncology, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC H2W 1R7, Canada., Li B; Laboratory of Molecular Oncology, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC H2W 1R7, Canada; Molecular Biology Program, University of Montréal, Montréal, QC H3T 1J4, Canada., Ruzsics Z; Institute of Virology, University Medical Center, Faculty of Medicine, University of Freiburg, 79104 Freiburg, Germany., Lau CM; Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA., O'Sullivan TE; Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA., Vidal SM; Department of Human Genetics, McGill University, Montréal, QC H3A 0C7, Canada; Dahdaleh Institute of Genomic Medicine, McGill University, Montréal, QC H3A 0G1, Canada., Sun JC; Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Department of Immunology and Microbial Pathogenesis, Weill Cornell Medical College, New York, NY 10065, USA., Veillette A; Laboratory of Molecular Oncology, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, QC H2W 1R7, Canada; Department of Medicine, McGill University, Montréal, QC H3G 1Y6, Canada; Molecular Biology Program, University of Montréal, Montréal, QC H3T 1J4, Canada. Electronic address: andre.veillette@ircm.qc.ca.
Jazyk:	angličtina
Zdroj:	Cell reports [Cell Rep] 2024 Mar 26; Vol. 43 (3), pp. 113800. Date of Electronic Publication: 2024 Feb 21.
DOI:	10.1016/j.celrep.2024.113800
Abstrakt:	Infection of mice by mouse cytomegalovirus (MCMV) triggers activation and expansion of Ly49H + natural killer (NK) cells, which are virus specific and considered to be "adaptive" or "memory" NK cells. Here, we find that signaling lymphocytic activation molecule family receptors (SFRs), a group of hematopoietic cell-restricted receptors, are essential for the expansion of Ly49H + NK cells after MCMV infection. This activity is largely mediated by CD48, an SFR broadly expressed on NK cells and displaying augmented expression after MCMV infection. It is also dependent on the CD48 counter-receptor, 2B4, expressed on host macrophages. The 2B4-CD48 axis promotes expansion of Ly49H + NK cells by repressing their phagocytosis by virus-activated macrophages through inhibition of the pro-phagocytic integrin lymphocyte function-associated antigen-1 (LFA-1) on macrophages. These data identify key roles of macrophages and the 2B4-CD48 pathway in controlling the expansion of adaptive NK cells following MCMV infection. Stimulation of the 2B4-CD48 axis may be helpful in enhancing adaptive NK cell responses for therapeutic purposes. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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