PMID- 28424684
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230201
IS  - 1664-3224 (Print)
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 8
DP  - 2017
TI  - Modulation of Human Leukocyte Antigen-C by Human Cytomegalovirus Stimulates 
      KIR2DS1 Recognition by Natural Killer Cells.
PG  - 298
LID - 10.3389/fimmu.2017.00298 [doi]
LID - 298
AB  - The interaction of inhibitory killer cell Ig-like receptors (KIRs) with human 
      leukocyte antigen (HLA) class I molecules has been characterized in detail. By 
      contrast, activating members of the KIR family, although closely related to 
      inhibitory KIRs, appear to interact weakly, if at all, with HLA class I. KIR2DS1 
      is the best studied activating KIR and it interacts with C2 group HLA-C 
      (C2-HLA-C) in some assays, but not as strongly as KIR2DL1. We used a mouse 2B4 
      cell reporter system, which carries NFAT-green fluorescent protein with KIR2DS1 
      and a modified DAP12 adaptor protein. KIR2DS1 reporter cells were not activated 
      upon coculture with 721.221 cells transfected with different HLA-C molecules, or 
      with interferon-gamma stimulated primary dermal fibroblasts. However, KIR2DS1 
      reporter cells and KIR2DS1(+) primary natural killer (NK) cells were activated by 
      C2-HLA-C homozygous human fetal foreskin fibroblasts (HFFFs) but only after 
      infection with specific clones of a clinical strain of human cytomegalovirus 
      (HCMV). Active viral gene expression was required for activation of both cell 
      types. Primary NKG2A(-)KIR2DS1(+) NK cell subsets degranulated after coculture 
      with HCMV-infected HFFFs. The W6/32 antibody to HLA class I blocked the KIR2DS1 
      reporter cell interaction with its ligand on HCMV-infected HFFFs but did not 
      block interaction with KIR2DL1. This implies a differential recognition of HLA-C 
      by KIR2DL1 and KIR2DS1. The data suggest that modulation of HLA-C by HCMV is 
      required for a potent KIR2DS1-mediated NK cell activation.
FAU - van der Ploeg, Kattria
AU  - van der Ploeg K
AD  - Department of Pathology, University of Cambridge, Cambridge, UK.
FAU - Chang, Chiwen
AU  - Chang C
AD  - Department of Pathology, University of Cambridge, Cambridge, UK.
FAU - Ivarsson, Martin A
AU  - Ivarsson MA
AD  - Department of Pathology, University of Cambridge, Cambridge, UK.
FAU - Moffett, Ashley
AU  - Moffett A
AD  - Department of Pathology, University of Cambridge, Cambridge, UK.
FAU - Wills, Mark R
AU  - Wills MR
AD  - Department of Medicine, University of Cambridge, Cambridge, UK.
FAU - Trowsdale, John
AU  - Trowsdale J
AD  - Department of Pathology, University of Cambridge, Cambridge, UK.
LA  - eng
GR  - G0701279/MRC_/Medical Research Council/United Kingdom
GR  - MR/K021087/1/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
DEP - 20170329
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
PMC - PMC5372792
OTO - NOTNLM
OT  - HLA-C
OT  - KIR2DS1
OT  - human cytomegalovirus
OT  - killer Ig-like receptor
OT  - natural killer cells
EDAT- 2017/04/21 06:00
MHDA- 2017/04/21 06:01
PMCR- 2017/01/01
CRDT- 2017/04/21 06:00
PHST- 2017/01/20 00:00 [received]
PHST- 2017/03/03 00:00 [accepted]
PHST- 2017/04/21 06:00 [entrez]
PHST- 2017/04/21 06:00 [pubmed]
PHST- 2017/04/21 06:01 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2017.00298 [doi]
PST - epublish
SO  - Front Immunol. 2017 Mar 29;8:298. doi: 10.3389/fimmu.2017.00298. eCollection 
      2017.