PMID- 26244383
OWN - NLM
STAT- MEDLINE
DCOM- 20160426
LR  - 20150806
IS  - 1473-5571 (Electronic)
IS  - 0269-9370 (Linking)
VI  - 29
IP  - 12
DP  - 2015 Jul 31
TI  - Natural killer cell education does not affect the magnitude of granzyme B 
      delivery to target cells by antibody-dependent cellular cytotoxicity.
PG  - 1433-43
LID - 10.1097/QAD.0000000000000729 [doi]
AB  - OBJECTIVE: Interest in the role of antibody-dependent cellular cytotoxicity 
      (ADCC) in protection from HIV infection has grown since analyses of the RV144 HIV 
      vaccine trial results found ADCC correlated with protection. Natural killer (NK) 
      cells are among the effector cells that mediate ADCC. The level of 
      antibody-induced NK cell activation depends on NK cell education through 
      inhibitory NK cell receptor human leukocyte antigen (HLA) ligand interactions. 
      Here, we investigated the impact of NK cell education on the delivery of Granzyme 
      B (GzB) to target cells. DESIGN: Lymphocytes from 50 HIV-uninfected [30 Bw4 (Bw4) 
      and 20 Bw4 (Bw6)] KIR3DL1 homozygote persons were used as effectors and 
      cocultured with gp120-coated target cells in the presence of a single source of 
      anti-HIV gp120 antibody to ascertain whether NK cell education status influenced 
      the level of GzB delivered to target cells. METHODS: The GTL assay assessed the 
      frequency of GzB-positive (%GzB) CEM.NKr.CCR5 target cells generated by effectors 
      from each individual. The frequency of CD107a, interferon (IFN)-gamma and CCL4 NK 
      cells was assessed as a measure of antibody-induced NK cell activation. RESULTS: 
      KIR3DL1 NK cells from the Bw4 group were more functional than KIR3DL1 NK cells. 
      Despite this, the %GzB target cells generated in the GTL assay did not differ 
      according to the KIR3DL1-HLA-B genotype of the effector cells. The %GzB cells 
      positively correlated with the frequency of CD16KIR3DL1 NK cells in the effector 
      population. CONCLUSION: ADCC potency does not depend on NK cell education.
FAU - Isitman, Gamze
AU  - Isitman G
AD  - aResearch Institute of the McGill University Health Centre (RI-MUHC) bDivision of 
      Experimental Medicine, McGill University, Montreal, Quebec, Canada cDepartment of 
      Microbiology and Immunology at the Peter Doherty Institute, University of 
      Melbourne, Melbourne, Victoria, Australia. dCentre de Recherche du Centre 
      Hospitalier de l'Universite de Montreal (CRCHUM) eMcGill AIDS Center, Lady Davis 
      Institute, Jewish General Hospital, McGill University fDepartment of Family 
      Medicine, Universite de Montreal gChronic Viral Illness Service hDivision of 
      Clinical Immunology, McGill University Health Centre, Montreal, Quebec, Canada.
FAU - Lisovsky, Irene
AU  - Lisovsky I
FAU - Tremblay-McLean, Alexandra
AU  - Tremblay-McLean A
FAU - Parsons, Matthew S
AU  - Parsons MS
FAU - Shoukry, Naglaa H
AU  - Shoukry NH
FAU - Wainberg, Mark A
AU  - Wainberg MA
FAU - Bruneau, Julie
AU  - Bruneau J
FAU - Bernard, Nicole F
AU  - Bernard NF
LA  - eng
GR  - MOP-123800/Canadian Institutes of Health Research/Canada
GR  - THA-118628/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
RN  - 0 (CCL4 protein, human)
RN  - 0 (Chemokine CCL4)
RN  - 0 (HIV Antibodies)
RN  - 0 (Lysosomal-Associated Membrane Protein 1)
RN  - 82115-62-6 (Interferon-gamma)
RN  - EC 3.4.21.- (Granzymes)
SB  - IM
MH  - *Antibody-Dependent Cell Cytotoxicity
MH  - Cells, Cultured
MH  - Chemokine CCL4/analysis
MH  - Granzymes/*metabolism
MH  - HIV Antibodies/*immunology
MH  - HIV Infections/*immunology
MH  - Humans
MH  - Immunophenotyping
MH  - Interferon-gamma/analysis
MH  - Killer Cells, Natural/*immunology
MH  - Lysosomal-Associated Membrane Protein 1/analysis
EDAT- 2015/08/06 06:00
MHDA- 2016/04/27 06:00
CRDT- 2015/08/06 06:00
PHST- 2015/08/06 06:00 [entrez]
PHST- 2015/08/06 06:00 [pubmed]
PHST- 2016/04/27 06:00 [medline]
AID - 00002030-201507310-00003 [pii]
AID - 10.1097/QAD.0000000000000729 [doi]
PST - ppublish
SO  - AIDS. 2015 Jul 31;29(12):1433-43. doi: 10.1097/QAD.0000000000000729.