Publikation

FOXP3 expression in hepatitis C virus-specific CD4+ T cells during acute hepatitis C

Wissenschaftlicher Artikel/Review - 01.10.2009

Bereiche
PubMed
DOI

Zitation
Heeg M, Spannagl M, Kauke T, Horster S, Schraut W, Raziorrouh B, Gerlach T, Jung M, Zachoval R, Grüner N, Ulsenheimer A, Diepolder H. FOXP3 expression in hepatitis C virus-specific CD4+ T cells during acute hepatitis C. Gastroenterology 2009; 137:1280-8.e1-6.
Art
Wissenschaftlicher Artikel/Review (Englisch)
Zeitschrift
Gastroenterology 2009; 137
Veröffentlichungsdatum
01.10.2009
eISSN (Online)
1528-0012
Seiten
1280-8.e1-6
Kurzbeschreibung/Zielsetzung

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.