PMID- 26647083
OWN - NLM
STAT- MEDLINE
DCOM- 20160720
LR  - 20220317
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 184
IP  - 1
DP  - 2016 Apr
TI  - Functional advantage of educated KIR2DL1(+) natural killer cells for anti-HIV-1 
      antibody-dependent activation.
PG  - 101-9
LID - 10.1111/cei.12752 [doi]
AB  - Evidence from the RV144 HIV-1 vaccine trial implicates anti-HIV-1 
      antibody-dependent cellular cytotoxicity (ADCC) in vaccine-conferred protection 
      from infection. Among effector cells that mediate ADCC are natural killer (NK) 
      cells. The ability of NK cells to be activated in an antibody-dependent manner is 
      reliant upon several factors. In general, NK cell-mediated antibody-dependent 
      activation is most robust in terminally differentiated CD57(+) NK cells, as well 
      as NK cells educated through ontological interactions between inhibitory killer 
      immunoglobulin-like receptors (KIR) and their major histocompatibility complex 
      class I [MHC-I or human leucocyte antigen (HLA-I)] ligands. With regard to 
      anti-HIV-1 antibody-dependent NK cell activation, previous research has 
      demonstrated that the epidemiologically relevant KIR3DL1/HLA-Bw4 receptor/ligand 
      combination confers enhanced activation potential. In the present study we 
      assessed the ability of the KIR2DL1/HLA-C2 receptor/ligand combination to confer 
      enhanced activation upon direct stimulation with HLA-I-devoid target cells or 
      antibody-dependent stimulation with HIV-1 gp140-pulsed CEM.NKr-CCR5 target cells 
      in the presence of an anti-HIV-1 antibody source. Among donors carrying the 
      HLA-C2 ligand for KIR2DL1, higher interferon (IFN)-gamma production was observed 
      within KIR2DL1(+) NK cells than in KIR2DL1(-) NK cells upon both direct and 
      antibody-dependent stimulation. No differences in KIR2DL1(+) and KIR2DL1(-) NK 
      cell activation were observed in HLA-C1 homozygous donors. Additionally, higher 
      activation in KIR2DL1(+) than KIR2DL1(-) NK cells from HLA-C2 carrying donors was 
      observed within less differentiated CD57(-) NK cells, demonstrating that the 
      observed differences were due to education and not an overabundance of KIR2DL1(+) 
      NK cells within differentiated CD57(+) NK cells. These observations are relevant 
      for understanding the regulation of anti-HIV-1 antibody-dependent NK cell 
      responses.
CI  - (c) 2016 British Society for Immunology.
FAU - Gooneratne, S L
AU  - Gooneratne SL
AD  - Department of Microbiology and Immunology, Peter Doherty Institute for Infection 
      and Immunity, University of Melbourne, Melbourne, VIC, Australia.
FAU - Center, R J
AU  - Center RJ
AD  - Centre for Biomedical Research, Burnet Institute, Melbourne, VIC, Australia.
FAU - Kent, S J
AU  - Kent SJ
AD  - Department of Microbiology and Immunology, Peter Doherty Institute for Infection 
      and Immunity, University of Melbourne, Melbourne, VIC, Australia.
AD  - Melbourne Sexual Health Centre, Carlton, VIC, Australia.
AD  - ARC Centre of Excellence in Convergent Bio-Nano Science and Technology, 
      University of Melbourne, Melbourne, VIC, Australia.
FAU - Parsons, M S
AU  - Parsons MS
AD  - Department of Microbiology and Immunology, Peter Doherty Institute for Infection 
      and Immunity, University of Melbourne, Melbourne, VIC, Australia.
LA  - eng
PT  - Journal Article
DEP - 20160204
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (CD57 Antigens)
RN  - 0 (HIV Antibodies)
RN  - 0 (HLA-C Antigens)
RN  - 0 (KIR2DL1 protein, human)
RN  - 0 (Receptors, KIR2DL1)
RN  - 0 (Recombinant Proteins)
RN  - 0 (env Gene Products, Human Immunodeficiency Virus)
RN  - 0 (gp140 envelope protein, Human immunodeficiency virus 1)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Alleles
MH  - CD4-Positive T-Lymphocytes/drug effects/immunology/virology
MH  - CD57 Antigens/genetics/immunology
MH  - Gene Expression
MH  - HIV Antibodies/*biosynthesis/pharmacology
MH  - HIV Infections/immunology/virology
MH  - HIV-1/*immunology
MH  - HLA-C Antigens/classification/genetics/*immunology
MH  - Histocompatibility Testing
MH  - Humans
MH  - *Immunity, Humoral
MH  - Immunologic Memory/drug effects
MH  - Interferon-gamma/biosynthesis/immunology
MH  - Killer Cells, Natural/*drug effects/immunology/virology
MH  - Lymphocyte Activation/drug effects
MH  - Primary Cell Culture
MH  - Receptors, KIR2DL1/deficiency/genetics/*immunology
MH  - Recombinant Proteins/genetics/immunology/pharmacology
MH  - env Gene Products, Human Immunodeficiency Virus/genetics/immunology/pharmacology
PMC - PMC4778096
OTO - NOTNLM
OT  - AIDS
OT  - killer immunoglobulin-like receptors
OT  - natural killer cells
EDAT- 2015/12/10 06:00
MHDA- 2016/07/21 06:00
PMCR- 2017/04/01
CRDT- 2015/12/10 06:00
PHST- 2015/07/08 00:00 [received]
PHST- 2015/11/13 00:00 [revised]
PHST- 2015/11/25 00:00 [accepted]
PHST- 2015/12/10 06:00 [entrez]
PHST- 2015/12/10 06:00 [pubmed]
PHST- 2016/07/21 06:00 [medline]
PHST- 2017/04/01 00:00 [pmc-release]
AID - CEI12752 [pii]
AID - 10.1111/cei.12752 [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2016 Apr;184(1):101-9. doi: 10.1111/cei.12752. Epub 2016 Feb 4.