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Blood, 1 May 2004, Vol. 103, No. 9, pp. 3428-3430. Prepublished online as a Blood First Edition Paper on December 18, 2003; DOI 10.1182/blood-2003-07-2598. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-07-2598v1 103/9/3428    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Boyer, O. Articles by Klatzmann, D. Search for Related Content PubMed PubMed Citation Articles by Boyer, O. Articles by Klatzmann, D. Related Collections Immunobiology Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY CD4+CD25+ regulatory T-cell deficiency in patients with hepatitis C-mixed cryoglobulinemia vasculitis Olivier Boyer, David Saadoun, Julien Abriol, Mélanie Dodille, Jean-Charles Piette, Patrice Cacoub, and David Klatzmann From the Laboratoire de Biologie et Thérapeutique des Pathologies Immunitaires, CNRS/UPMC UMR 7087 and Service de Médecine Interne, Hôpital Pitié-Salpêtrière, Paris, France. 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+CD25high 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. 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