PMID- 37140380
OWN - NLM
STAT- MEDLINE
DCOM- 20230629
LR  - 20230702
IS  - 1470-8752 (Electronic)
IS  - 0300-5127 (Linking)
VI  - 51
IP  - 3
DP  - 2023 Jun 28
TI  - The CD56-CD16+ NK cell subset in chronic infections.
PG  - 1201-1212
LID - 10.1042/BST20221374 [doi]
AB  - Long-term human diseases can shape the immune system, and natural killer (NK) 
      cells have been documented to differentiate into distinct subsets specifically 
      associated with chronic virus infections. One of these subsets found in large 
      frequencies in HIV-1 are the CD56-CD16+ NK cells, and this population's 
      association with chronic virus infections is the subject of this review. Human NK 
      cells are classically defined by CD56 expression, yet increasing evidence 
      supports the NK cell status of the CD56-CD16+ subset which we discuss herein. We 
      then discuss the evidence linking CD56-CD16+ NK cells to chronic virus 
      infections, and the potential immunological pathways that are altered by 
      long-term infection that could be inducing the population's differentiation. An 
      important aspect of NK cell regulation is their interaction with human leukocyte 
      antigen (HLA) class-I molecules, and we highlight work that indicates both virus 
      and genetic-mediated variations in HLA expression that have been linked to 
      CD56-CD16+ NK cell frequencies. Finally, we offer a perspective on CD56-CD16+ NK 
      cell function, taking into account recent work that implies the subset is 
      comparable to CD56+CD16+ NK cell functionality in antibody-dependent cell 
      cytotoxicity response, and the definition of CD56-CD16+ NK cell subpopulations 
      with varying degranulation capacity against target cells.
CI  - (c) 2023 The Author(s). Published by Portland Press Limited on behalf of the 
      Biochemical Society.
FAU - Cocker, Alexander T H
AU  - Cocker ATH
AUID- ORCID: 0000-0001-7162-0774
AD  - Department of Structural Biology, Stanford University School of Medicine, 
      Stanford, CA, U.S.A.
AD  - Department of Microbiology and Immunology, Stanford University School of 
      Medicine, Stanford, CA, U.S.A.
FAU - Guethlein, Lisbeth A
AU  - Guethlein LA
AD  - Department of Structural Biology, Stanford University School of Medicine, 
      Stanford, CA, U.S.A.
AD  - Department of Microbiology and Immunology, Stanford University School of 
      Medicine, Stanford, CA, U.S.A.
FAU - Parham, Peter
AU  - Parham P
AD  - Department of Structural Biology, Stanford University School of Medicine, 
      Stanford, CA, U.S.A.
AD  - Department of Microbiology and Immunology, Stanford University School of 
      Medicine, Stanford, CA, U.S.A.
LA  - eng
GR  - R01 AI136952/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Biochem Soc Trans
JT  - Biochemical Society transactions
JID - 7506897
RN  - 0 (CD56 Antigen)
RN  - 0 (Receptors, IgG)
SB  - IM
MH  - Humans
MH  - *Persistent Infection
MH  - CD56 Antigen/metabolism
MH  - Receptors, IgG/metabolism
MH  - Killer Cells, Natural/metabolism
MH  - *Virus Diseases/metabolism
OTO - NOTNLM
OT  - CD56-CD16+
OT  - HIV-1
OT  - NK cells
OT  - chronic virus
OT  - function
OT  - regulation
EDAT- 2023/05/04 12:41
MHDA- 2023/06/29 06:43
CRDT- 2023/05/04 10:04
PHST- 2023/02/09 00:00 [received]
PHST- 2023/04/14 00:00 [revised]
PHST- 2023/04/18 00:00 [accepted]
PHST- 2023/06/29 06:43 [medline]
PHST- 2023/05/04 12:41 [pubmed]
PHST- 2023/05/04 10:04 [entrez]
AID - 233017 [pii]
AID - 10.1042/BST20221374 [doi]
PST - ppublish
SO  - Biochem Soc Trans. 2023 Jun 28;51(3):1201-1212. doi: 10.1042/BST20221374.