Natural killer cells in hepatitis C: Current progress

doi:10.3748/wjg.v22.i4.1449

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Jan 28, 2016 (publication date) through Nov 25, 2024

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastroenterol. Jan 28, 2016; 22(4): 1449-1460
Published online Jan 28, 2016. doi: 10.3748/wjg.v22.i4.1449

Table 1 Controversies over phenotype and function of natural killer cells in chronic hepatitis C virus infection

Phenotype/function	Ref. reported increase	Ref. reported decrease	Ref. reported no change
Activation marker
CD69	[34]		[88]
Activating receptor
NKG2D	[34]	[68]
NKG2C	[77]
NKp46	[77,88,89]	[80]
NKp30	[88]	[80]
NKp44	[77]
Inhibitory receptor
KIR3DL1		[34]
NKG2A	[78-80]
KLRG1	[90]
Cytotoxicity
Degranulation	[34,77]	[68,80,89]	[78]
TRAIL expression	[77]	[89]
Immunostimulating cytokine
IFN-γ	[78]	[34,68]	[77,88]
Immunosuppressive cytokine
IL-10	[88]

IL: Interleukin; IFN: Interferon; NKG2D: Natural killer group 2D; TRAIL: Factor-related apoptosis inducing ligand; KLRG1: Killer cell lectin-like receptor subfamily G member 1.

Citation: Yoon JC, Yang CM, Song Y, Lee JM. Natural killer cells in hepatitis C: Current progress. World J Gastroenterol 2016; 22(4): 1449-1460
URL: https://www.wjgnet.com/1007-9327/full/v22/i4/1449.htm
DOI: https://dx.doi.org/10.3748/wjg.v22.i4.1449