PMID- 36599262
OWN - NLM
STAT- MEDLINE
DCOM- 20230307
LR  - 20230316
IS  - 1878-3279 (Electronic)
IS  - 0171-2985 (Linking)
VI  - 228
IP  - 2
DP  - 2023 Mar
TI  - The impact of killer cell immunoglobulin-like receptor (KIR) genes and human 
      leukocyte antigen (HLA) class I ligands on predisposition or protection against 
      prostate cancer.
PG  - 152319
LID - S0171-2985(22)00145-0 [pii]
LID - 10.1016/j.imbio.2022.152319 [doi]
AB  - Natural killer (NK) cell development largely depends on killer cell 
      immunoglobulin-like receptors (KIRs) and human leukocyte antigen (HLA) class I 
      ligands. In the current study, we investigated the role of KIR genes, HLA 
      ligands, and KIR-HLA combinations in vulnerability or protection against prostate 
      cancer (PC). To analyze the frequency of 16 KIR genes and 5 HLA ligands, 
      polymerase chain reaction with sequence-specific primers (PCR-SSP) was conducted 
      in 150 PC patients and 200 healthy controls (CNs). KIR2DL5 (p = 0.0346, 
      OR = 0.606, CI = 0.3916-0.9336), KIR2DS5 (p = 0.0227, OR = 0.587, 
      CI = 0.3793-0.9139), HLA-B Bw4(Thr80) (p = 0.0401, OR = 0.3552, 
      CI = 0.1466-0.9059), HLA Bw4 (p = 0.0190, OR = 0.4744, CI = 0.2656-0.8521), and 
      T4 gene cluster (including KIR2DS5-2DL5-3DS1-2DS1 genes) (p = 0.0194, 
      OR = 0.5575, CI = 0.3449-0.8938) had a lower frequency in the PC patients 
      compared to the control group. Moreover, a lower frequency of the genotypes 
      contacting activating KIR (aKIR) > inhibitory KIR (iKIR) (p = 0.0298, 
      OR = 0.5291, CI = 0.3056-0.9174) and iKIR + HLA < aKIR + HLA (p = 0.0183, 
      OR = 0.2197, CI = 0.0672-0.7001) in PC patients compared to the CNs implies a 
      protective role for aKIR genes. In the case of KIR-HLA interactions, we detected 
      a significant association between KIR3DS1(+) + HLA-A Bw4(+) (p = 0.0113, 
      OR = 0.5093, CI = 0.3124-0.8416) and KIR3DL1(-) + HLA-A Bw4(+) (p = 0.0306, 
      OR = 0.1153, CI = 0.0106-0.6537) combinations and resistance to prostate cancer. 
      In contrast, the presence of KIR3DL1 in the absence of HLA-A Bw4 (p = 0.0040, 
      OR = 2.00, CI = 1.264-3.111), HLA Bw4 (p = 0.0296, OR = 2.066, CI = 1.094-3.906), 
      and HLA-Bw4(Thr80) (p = 0.0071, OR = 2.505, CI = 1.319-4.703) genes probably 
      predisposes to prostate cancer. Carrying the CxT4 genotype in PC patients was 
      positively associated with lower tumor grades (Gleason score </= 6) (p = 0.0331, 
      OR = 3.290, and CI = 1.181-8.395). Altogether, our data suggest a protective role 
      for aKIRs, HLA-B Bw4(Thr80), and HLA Bw4 ligands as well as a predisposing role 
      for certain KIR-HLA combinations in prostate cancer. The findings of this study 
      offer new insight into the population's risk assessment for prostate cancer in 
      men. Additionally, predicting immunotherapy response based on KIR-HLA 
      combinations aids in implementing the most effective therapeutic approach in the 
      early stages of the disease.
CI  - Copyright (c) 2023 Elsevier GmbH. All rights reserved.
FAU - Roshan Zamir, Mina
AU  - Roshan Zamir M
AD  - Department of Immunology, School of Medicine, Tehran University of Medical 
      Sciences, Tehran, Iran; Shiraz Institute for Cancer Research, School of Medicine, 
      Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address: 
      minarzs95@gmail.com.
FAU - Ariafar, Ali
AU  - Ariafar A
AD  - Urology-Oncology Research Center, Shiraz University of Medical Sciences, Shiraz, 
      Iran; Department of Urology, School of Medicine, Shiraz University of Medical 
      Sciences, Shiraz, Iran. Electronic address: ariafara@sums.ac.ir.
FAU - Ghaderi, Abbas
AU  - Ghaderi A
AD  - Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of 
      Medical Sciences, Shiraz, Iran; Department of Immunology, School of Medicine, 
      Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address: 
      ghaderia@sums.ac.ir.
FAU - Amirzargar, Aliakbar
AU  - Amirzargar A
AD  - Department of Immunology, School of Medicine, Tehran University of Medical 
      Sciences, Tehran, Iran. Electronic address: amirzara@tums.ac.ir.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20221227
PL  - Netherlands
TA  - Immunobiology
JT  - Immunobiology
JID - 8002742
RN  - 0 (Ligands)
RN  - 0 (Receptors, KIR)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (HLA-B Antigens)
RN  - 0 (HLA Antigens)
RN  - 0 (HLA-A Antigens)
SB  - IM
MH  - Male
MH  - Humans
MH  - Ligands
MH  - Gene Frequency
MH  - *Receptors, KIR/genetics
MH  - Genotype
MH  - Histocompatibility Antigens Class I/genetics
MH  - HLA-B Antigens
MH  - HLA Antigens/genetics
MH  - Disease Susceptibility
MH  - HLA-A Antigens/genetics
MH  - *Prostatic Neoplasms
OTO - NOTNLM
OT  - HLA
OT  - KIR
OT  - KIR-HLA interaction
OT  - NK cell
OT  - PCR-SSP
OT  - Prostate cancer
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/01/05 06:00
MHDA- 2023/03/08 06:00
CRDT- 2023/01/04 18:11
PHST- 2022/08/20 00:00 [received]
PHST- 2022/12/02 00:00 [revised]
PHST- 2022/12/24 00:00 [accepted]
PHST- 2023/01/05 06:00 [pubmed]
PHST- 2023/03/08 06:00 [medline]
PHST- 2023/01/04 18:11 [entrez]
AID - S0171-2985(22)00145-0 [pii]
AID - 10.1016/j.imbio.2022.152319 [doi]
PST - ppublish
SO  - Immunobiology. 2023 Mar;228(2):152319. doi: 10.1016/j.imbio.2022.152319. Epub 
      2022 Dec 27.