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FOXP3 expression in hepatitis C virus-specific CD4+ T cells during acute hepatitis C.
Gastroenterology. 2009 Oct; 137(4):1280-8.e1-6.G

Abstract

BACKGROUND & AIMS

Down-regulation of hepatitis C virus (HCV)-specific CD4(+) T-cell responses is a hallmark of chronic viral persistence in acute hepatitis C. FOXP3(+)CD25(+)CD4(+) regulatory T cells can modulate HCV-specific immune responses in vitro, but the role of virus-specific regulatory T cells in the pathogenesis of chronic viral persistence is unknown.

METHODS

Two novel HLA-DR15 tetramers were synthesized to study the kinetics and phenotype of FOXP3(+)-expressing HCV-specific CD4(+) T cells from 10 patients with acute hepatitis C and 15 patients with chronic hepatitis C.

RESULTS

In acute hepatitis C, generally only a low percentage of HCV-specific CD4(+) T cells expressed FOXP3(+) (mean of 2.5% in patients with self-limited acute hepatitis C vs 2.4% in patients with evolving chronic hepatitis C). Although distinct but short-lived increases in virus-specific FOXP3(+)CD4(+) T cells occurred in 3 patients (30%, 26%, and 7% of tet(+) CD4(+) T cells, respectively), these did not correlate with the evolution of chronic hepatitis C. HCV-specific FOXP3(+)CD4(+) T cells displayed a distinct phenotype, with only 10% expressing CD25 and 40% being CD127low. Interestingly, this phenotype of FOXP3(+)CD4(+) T cells was already expanded in bulk CD4(+) T cells in patients with chronic hepatitis C.

CONCLUSIONS

Although short-lived increases in HCV-specific FOXP3(+)CD4(+) T cells occur during the course of acute hepatitis C, we could not demonstrate an association of HCV-specific regulatory T cells and persistent viremia.

Authors+Show Affiliations

Medical Department II and Institute for Immunology, Ludwig-Maximilians-University Munich, Munich, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19596013

Citation

Heeg, Malte H J., et al. "FOXP3 Expression in Hepatitis C Virus-specific CD4+ T Cells During Acute Hepatitis C." Gastroenterology, vol. 137, no. 4, 2009, pp. 1280-8.e1-6.
Heeg MH, Ulsenheimer A, Grüner NH, et al. FOXP3 expression in hepatitis C virus-specific CD4+ T cells during acute hepatitis C. Gastroenterology. 2009;137(4):1280-8.e1-6.
Heeg, M. H., Ulsenheimer, A., Grüner, N. H., Zachoval, R., Jung, M. C., Gerlach, J. T., Raziorrouh, B., Schraut, W., Horster, S., Kauke, T., Spannagl, M., & Diepolder, H. M. (2009). FOXP3 expression in hepatitis C virus-specific CD4+ T cells during acute hepatitis C. Gastroenterology, 137(4), 1280-e1-6. https://doi.org/10.1053/j.gastro.2009.06.059
Heeg MH, et al. FOXP3 Expression in Hepatitis C Virus-specific CD4+ T Cells During Acute Hepatitis C. Gastroenterology. 2009;137(4):1280-8.e1-6. PubMed PMID: 19596013.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - FOXP3 expression in hepatitis C virus-specific CD4+ T cells during acute hepatitis C. AU - Heeg,Malte H J, AU - Ulsenheimer,Axel, AU - Grüner,Norbert H, AU - Zachoval,Reinhart, AU - Jung,Maria-Christina, AU - Gerlach,J Tilman, AU - Raziorrouh,Bijan, AU - Schraut,Winfried, AU - Horster,Sophia, AU - Kauke,Teresa, AU - Spannagl,Michael, AU - Diepolder,Helmut M, Y1 - 2009/07/29/ PY - 2008/06/25/received PY - 2009/06/17/revised PY - 2009/06/29/accepted PY - 2009/7/15/entrez PY - 2009/7/15/pubmed PY - 2009/10/16/medline SP - 1280-8.e1-6 JF - Gastroenterology JO - Gastroenterology VL - 137 IS - 4 N2 - BACKGROUND & AIMS: Down-regulation of hepatitis C virus (HCV)-specific CD4(+) T-cell responses is a hallmark of chronic viral persistence in acute hepatitis C. FOXP3(+)CD25(+)CD4(+) regulatory T cells can modulate HCV-specific immune responses in vitro, but the role of virus-specific regulatory T cells in the pathogenesis of chronic viral persistence is unknown. METHODS: Two novel HLA-DR15 tetramers were synthesized to study the kinetics and phenotype of FOXP3(+)-expressing HCV-specific CD4(+) T cells from 10 patients with acute hepatitis C and 15 patients with chronic hepatitis C. RESULTS: In acute hepatitis C, generally only a low percentage of HCV-specific CD4(+) T cells expressed FOXP3(+) (mean of 2.5% in patients with self-limited acute hepatitis C vs 2.4% in patients with evolving chronic hepatitis C). Although distinct but short-lived increases in virus-specific FOXP3(+)CD4(+) T cells occurred in 3 patients (30%, 26%, and 7% of tet(+) CD4(+) T cells, respectively), these did not correlate with the evolution of chronic hepatitis C. HCV-specific FOXP3(+)CD4(+) T cells displayed a distinct phenotype, with only 10% expressing CD25 and 40% being CD127low. Interestingly, this phenotype of FOXP3(+)CD4(+) T cells was already expanded in bulk CD4(+) T cells in patients with chronic hepatitis C. CONCLUSIONS: Although short-lived increases in HCV-specific FOXP3(+)CD4(+) T cells occur during the course of acute hepatitis C, we could not demonstrate an association of HCV-specific regulatory T cells and persistent viremia. SN - 1528-0012 UR - https://www.unboundmedicine.com/medline/citation/19596013/FOXP3_expression_in_hepatitis_C_virus_specific_CD4+_T_cells_during_acute_hepatitis_C_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0016-5085(09)01147-0 DB - PRIME DP - Unbound Medicine ER -