Natural killer cells protect mice from DSS-induced colitis by regulating neutrophil function via the NKG2A receptor

Typeset version

 

TY  - JOUR
  - Hall, LJ,Murphy, CT,Quinlan, A,Hurley, G,Shanahan, F,Nally, K,Melgar, S
  - 2013
  - September
  - Mucosal immunology
  - Natural killer cells protect mice from DSS-induced colitis by regulating neutrophil function via the NKG2A receptor
  - Validated
  - Altmetric: 1 ()
  - INFLAMMATORY-BOWEL-DISEASE ACTIVE ULCERATIVE-COLITIS CD4(+) T-CELLS NK CELLS ADAPTIVE IMMUNITY ACTIVATION INNATE SURVIVAL MODEL DEFICIENT
  - 6
  - 1016
  - 1026
  - Natural killer (NK) cells are traditionally considered in the context of tumor surveillance and infection defense but their role in chronic inflammatory disorders such as inflammatory bowel disease is less clear. Here, we investigated the role of NK cells in dextran sodium sulfate (DSS)-induced colitis in mice. Depletion of NK cells impairs the survival of mice with colitis and is linked with dramatic increases in colonic damage, leukocyte infiltration, and pro-inflammatory profiles. Mice depleted of NK cells had increased numbers of neutrophils in colons and mesenteric lymph nodes, compared with control mice, in addition to acquiring a hyper-activation status. In vitro and in vivo studies demonstrate that NK cells downregulate pro-inflammatory functions of activated neutrophils, including reactive oxygen species and cytokine production, by direct cell-to-cell contact involving the NK cell-inhibitory receptor NKG2A. Our results indicate an immunoregulatory mechanism of action of NK cells attenuating DSS-induced colitis neutrophil-mediated inflammation and tissue injury via NKG2A-dependent mechanisms.
  - 10.1038/mi.2012.140
DA  - 2013/09
ER  - 
@article{V243943097,
   = {Hall,  LJ and Murphy,  CT and Quinlan,  A and Hurley,  G and Shanahan,  F and Nally,  K and Melgar,  S },
   = {2013},
   = {September},
   = {Mucosal immunology},
   = {Natural killer cells protect mice from DSS-induced colitis by regulating neutrophil function via the NKG2A receptor},
   = {Validated},
   = {Altmetric: 1 ()},
   = {INFLAMMATORY-BOWEL-DISEASE ACTIVE ULCERATIVE-COLITIS CD4(+) T-CELLS NK CELLS ADAPTIVE IMMUNITY ACTIVATION INNATE SURVIVAL MODEL DEFICIENT},
   = {6},
  pages = {1016--1026},
   = {{Natural killer (NK) cells are traditionally considered in the context of tumor surveillance and infection defense but their role in chronic inflammatory disorders such as inflammatory bowel disease is less clear. Here, we investigated the role of NK cells in dextran sodium sulfate (DSS)-induced colitis in mice. Depletion of NK cells impairs the survival of mice with colitis and is linked with dramatic increases in colonic damage, leukocyte infiltration, and pro-inflammatory profiles. Mice depleted of NK cells had increased numbers of neutrophils in colons and mesenteric lymph nodes, compared with control mice, in addition to acquiring a hyper-activation status. In vitro and in vivo studies demonstrate that NK cells downregulate pro-inflammatory functions of activated neutrophils, including reactive oxygen species and cytokine production, by direct cell-to-cell contact involving the NK cell-inhibitory receptor NKG2A. Our results indicate an immunoregulatory mechanism of action of NK cells attenuating DSS-induced colitis neutrophil-mediated inflammation and tissue injury via NKG2A-dependent mechanisms.}},
   = {10.1038/mi.2012.140},
  source = {IRIS}
}
AUTHORSHall, LJ,Murphy, CT,Quinlan, A,Hurley, G,Shanahan, F,Nally, K,Melgar, S
YEAR2013
MONTHSeptember
JOURNAL_CODEMucosal immunology
TITLENatural killer cells protect mice from DSS-induced colitis by regulating neutrophil function via the NKG2A receptor
STATUSValidated
TIMES_CITEDAltmetric: 1 ()
SEARCH_KEYWORDINFLAMMATORY-BOWEL-DISEASE ACTIVE ULCERATIVE-COLITIS CD4(+) T-CELLS NK CELLS ADAPTIVE IMMUNITY ACTIVATION INNATE SURVIVAL MODEL DEFICIENT
VOLUME6
ISSUE
START_PAGE1016
END_PAGE1026
ABSTRACTNatural killer (NK) cells are traditionally considered in the context of tumor surveillance and infection defense but their role in chronic inflammatory disorders such as inflammatory bowel disease is less clear. Here, we investigated the role of NK cells in dextran sodium sulfate (DSS)-induced colitis in mice. Depletion of NK cells impairs the survival of mice with colitis and is linked with dramatic increases in colonic damage, leukocyte infiltration, and pro-inflammatory profiles. Mice depleted of NK cells had increased numbers of neutrophils in colons and mesenteric lymph nodes, compared with control mice, in addition to acquiring a hyper-activation status. In vitro and in vivo studies demonstrate that NK cells downregulate pro-inflammatory functions of activated neutrophils, including reactive oxygen species and cytokine production, by direct cell-to-cell contact involving the NK cell-inhibitory receptor NKG2A. Our results indicate an immunoregulatory mechanism of action of NK cells attenuating DSS-induced colitis neutrophil-mediated inflammation and tissue injury via NKG2A-dependent mechanisms.
PUBLISHER_LOCATION
ISBN_ISSN
EDITION
URL
DOI_LINK10.1038/mi.2012.140
FUNDING_BODY
GRANT_DETAILS