Fachbereich Veterinärmedizin



    Defective suppressor function of human CD4+ CD25+ regulatory T cells in autoimmune polyglandular syndrome type II (2004)

    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Kriegel, Martin A
    Lohmann, Tobias
    Gabler, Christoph
    Blank, Norbert
    Kalden, Joachim R
    Lorenz, Hanns-Martin
    The Journal of Experimental Medicine; 199(9) — S. 1285–1291
    ISSN: 0022-1007
    Pubmed: 15117972
    Institut für Veterinär-Biochemie

    Oertzenweg 19 b
    14163 Berlin
    Tel.+49 30 838 62225 Fax.+49 30 838-62584

    Abstract / Zusammenfassung

    In autoimmune polyglandular syndromes (APS), several organ-specific autoimmune diseases are clustered. Although APS type I is caused by loss of central tolerance, the etiology of APS type II (APS-II) is currently unknown. However, in several murine models, depletion of CD4(+) CD25(+) regulatory T cells (T(regs)) causes a syndrome resembling human APS-II with multiple endocrinopathies. Therefore, we hypothesized that loss of active suppression in the periphery could be a hallmark of this syndrome. T(regs) from peripheral blood of APS-II, control patients with single autoimmune endocrinopathies, and normal healthy donors showed no differences in quantity (except for patients with isolated autoimmune diseases), in functionally important surface markers, or in apoptosis induced by growth factor withdrawal. Strikingly, APS-II T(regs) were defective in their suppressive capacity. The defect was persistent and not due to responder cell resistance. These data provide novel insights into the pathogenesis of APS-II and possibly human autoimmunity in general.