CD4+CD25+ regulatory T-cell deficiency in patients with hepatitis C-mixed cryoglobulinemia vasculitis

Blood. 2004 May 1;103(9):3428-30. doi: 10.1182/blood-2003-07-2598. Epub 2003 Dec 18.

Abstract

Patients who are chronically infected with hepatitis C virus (HCV) often develop mixed cryoglobulinemia (MC), a B-cell proliferative disorder with polyclonal activation and autoantibody production. We investigated if MC is associated with a deficit of CD4(+)CD25(+) immunoregulatory T (Treg) cells, which have been shown to control autoimmunity. Because Treg cells express higher amounts of CD25 than activated CD4(+) T cells, we analyzed blood CD4(+)CD25(high) Treg cells in 69 untreated patients chronically infected with HCV. Treg cell frequency in patients without MC (8.8% +/- 2.3%) or with asymptomatic MC (7.4% +/- 2.1%) was comparable to that of healthy controls (7.9% +/- 1.3%). In contrast, it was significantly reduced in symptomatic MC patients (2.6% +/- 1.2%, P <.001) even when compared to a panel of untreated HCV(-) patients with different inflammatory disorders (6.2% +/- 0.8%, P <.0001). In symptomatic MC patients, the purified remaining CD4(+)CD25(+) T cells retained suppressive activity in vitro. These results, together with experimental data showing that depletion of Treg cells induces autoimmunity, suggest a major role of Treg cell deficiency in HCV-MC vasculitis and this is the first report of a quantitative Treg cell deficiency in virus-associated autoimmunity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Autoimmunity
  • CD4 Lymphocyte Count
  • CD4-Positive T-Lymphocytes / pathology*
  • CD4-Positive T-Lymphocytes / virology
  • Case-Control Studies
  • Cryoglobulinemia / etiology*
  • Cryoglobulinemia / immunology
  • Cryoglobulinemia / virology
  • Hepatitis C / complications
  • Hepatitis C / immunology*
  • Humans
  • Middle Aged
  • Receptors, Interleukin-2*
  • T-Lymphocytes, Regulatory / pathology
  • T-Lymphocytes, Regulatory / virology
  • Vasculitis / etiology
  • Vasculitis / immunology
  • Vasculitis / virology

Substances

  • Receptors, Interleukin-2