PMID- 22566836
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20120823
LR  - 20211021
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 2
DP  - 2011
TI  - Modulation of the inhibitory receptor leukocyte Ig-like receptor 1 on human 
      natural killer cells.
PG  - 46
LID - 10.3389/fimmu.2011.00046 [doi]
LID - 46
AB  - Leukocyte Ig-like receptor 1 (LIR-1) is an inhibitory Ig superfamily receptor 
      with broad specificity for MHC-I expressed on leukocytes including natural killer 
      (NK) and T cells. The extent of LIR-1 expression on NK cells is quite disparate 
      between donors but the regulation of LIR-1 in NK cells is poorly understood. We 
      examined expression profiles of LIR-1 on NK and T lymphocytes in 11 healthy 
      donors over 1 year. Four of the 11 donors demonstrated substantial increases in 
      LIR-1(+) NK cells. High levels of LIR-1 expression were not correlated with 
      exposure to human cytomegalovirus or the fraction of CD57(+) NK cells in the donor. 
      LIR-1 levels on ex vivo NK and CD56(+) T cells were increased in vitro by short 
      term exposure to IL-2 or IL-15 compared to control but not with various other 
      cytokines tested. Sorted CD56(bright) NK cells also increased LIR-1 expression 
      when cultured in IL-2. Maintenance of LIR-1 on longer term NK cells was also 
      dependent on continuous stimulation by IL-15 or IL-2. While we could not detect 
      increases in total LIR-1 mRNA in response to cytokine treatment by qPCR, we 
      observed a shift in activity of LIR-1 promoter reporter constructs in the 
      presence of IL-2 favoring the more translationally active transcript from the 
      proximal promoter. Together these results show LIR-1 on NK cells is under the 
      control of cytokines known to drive NK cell maturation and activation and suggest 
      availability of such cytokines may alter the NK repertoire in vivo as we observed 
      in several donors with fluctuating levels of LIR-1 on their NK cells.
FAU - Li, Nicholas L
AU  - Li NL
AD  - Department of Medical Microbiology and Immunology, University of Alberta 
      Edmonton, AB, Canada.
FAU - Davidson, Chelsea L
AU  - Davidson CL
FAU - Humar, Atul
AU  - Humar A
FAU - Burshtyn, Deborah N
AU  - Burshtyn DN
LA  - eng
PT  - Journal Article
DEP - 20110920
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
PMC - PMC3342057
OTO - NOTNLM
OT  - LIR-1
OT  - inhibitory receptor
OT  - natural killer cells
EDAT- 2011/01/01 00:00
MHDA- 2011/01/01 00:01
PMCR- 2011/01/01
CRDT- 2012/05/09 06:00
PHST- 2011/06/22 00:00 [received]
PHST- 2011/09/05 00:00 [accepted]
PHST- 2012/05/09 06:00 [entrez]
PHST- 2011/01/01 00:00 [pubmed]
PHST- 2011/01/01 00:01 [medline]
PHST- 2011/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2011.00046 [doi]
PST - epublish
SO  - Front Immunol. 2011 Sep 20;2:46. doi: 10.3389/fimmu.2011.00046. eCollection 2011.