» Articles » PMID: 22183819

Interleukin (IL)-17/IL-22-producing T Cells Enriched Within the Liver of Patients with Chronic Hepatitis C Viral (HCV) Infection

Overview
Journal Dig Dis Sci
Specialty Gastroenterology
Date 2011 Dec 21
PMID 22183819
Citations 43
Authors
Affiliations
Soon will be listed here.
Abstract

Background: Effector CD4+ helper T cells have historically been classified into T helper 1 (Th1) and Th2 based on the production of signature cytokines. The recently identified interleukin (IL)-17 cytokine family plays important roles in host immunity against intracellular pathogens and in chronic inflammatory conditions; data have implicated IL-17 in autoimmune and viral liver disease.

Methods: This study used three patient groups with HCV infection: acute HCV who either cleared spontaneously or became chronically infected (n = 12), endstage liver disease from whom both peripheral and intrahepatic lymphocytes were studied directly ex vivo (n = 11), and 134 patients with different stages of HCV-related fibrosis from whom serum was collected concurrently with liver biopsy. Normal healthy subjects (n = 41) served as controls.

Results: Acute HCV was not associated with expansion of either CD4+ or CD8+ T cells producing IL-17 (Th17, Tc17) or IL-22, and frequencies did not differ in the blood of patients who cleared versus became persistently infected. The hepatic compartment of chronic HCV patients demonstrated statistically more CD4+ and CD8+ that produced IL-17, IL-22 or both as compared to peripheral blood. These T cells displayed a distinct phenotypic profile, high expression of the homing receptor CD161 and low levels of inhibitory receptors, mucin-domain-containing-molecule-3 (Tim-3) and programmed-death 1. Using a sensitive ELISA, we found no significant differences in serum levels of IL-17 according to HCV-related fibrosis.

Conclusions: In chronic HCV, T cells producing IL-17/IL-22 may home to the liver; however, circulating levels of IL-17 do not correlate with fibrosis.

Citing Articles

Biomarkers in Detection of Hepatitis C Virus Infection.

Woo J, Choi Y Pathogens. 2024; 13(4).

PMID: 38668286 PMC: 11054098. DOI: 10.3390/pathogens13040331.


Friend or Foe - Tc17 cell generation and current evidence for their importance in human disease.

Hipp A, Bengsch B, Globig A Discov Immunol. 2024; 2(1):kyad010.

PMID: 38567057 PMC: 10917240. DOI: 10.1093/discim/kyad010.


Unraveling IL-17 and IL-22 role in occult hepatitis C versus chronic hepatitis C virus infection.

Elbaz S, Mousa N, Elmetwalli A, Abdel-Razik A, Salah M, Elhammady A BMC Infect Dis. 2024; 24(1):134.

PMID: 38273234 PMC: 10811848. DOI: 10.1186/s12879-024-09032-6.


Human in vitro-induced IL-17A+ CD8+ T-cells exert pro-inflammatory effects on synovial fibroblasts.

Gray E, Srenathan U, Durham L, Lalnunhlimi S, Steel K, Catrina A Clin Exp Immunol. 2023; 214(1):103-119.

PMID: 37367825 PMC: 10711358. DOI: 10.1093/cei/uxad068.


Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.

Zhang K, Chen L, Zhu C, Zhang M, Liang C Pathogens. 2023; 12(2).

PMID: 36839448 PMC: 9965464. DOI: 10.3390/pathogens12020176.


References
1.
Wang C, Krantz E, Klarquist J, Krows M, McBride L, Scott E . Acute hepatitis C in a contemporary US cohort: modes of acquisition and factors influencing viral clearance. J Infect Dis. 2007; 196(10):1474-82. DOI: 10.1086/522608. View

2.
Davis G, Albright J, Cook S, Rosenberg D . Projecting future complications of chronic hepatitis C in the United States. Liver Transpl. 2003; 9(4):331-8. DOI: 10.1053/jlts.2003.50073. View

3.
Wolk K, Kunz S, Witte E, Friedrich M, Asadullah K, Sabat R . IL-22 increases the innate immunity of tissues. Immunity. 2004; 21(2):241-54. DOI: 10.1016/j.immuni.2004.07.007. View

4.
Kolls J, Khader S . The role of Th17 cytokines in primary mucosal immunity. Cytokine Growth Factor Rev. 2010; 21(6):443-8. PMC: 3004678. DOI: 10.1016/j.cytogfr.2010.11.002. View

5.
Lemmers A, Moreno C, Gustot T, Marechal R, Degre D, Demetter P . The interleukin-17 pathway is involved in human alcoholic liver disease. Hepatology. 2009; 49(2):646-57. DOI: 10.1002/hep.22680. View