The Journal of Experimental Medicine
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Published online 26 April 2004 doi:10.1084/jem.20032158
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 199, Number 9, 1285-1291
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Brief Definitive Report

 Defective Suppressor Function of Human CD4+ CD25+ Regulatory T Cells in Autoimmune Polyglandular Syndrome Type II

Martin A. Kriegel1, Tobias Lohmann2, Christoph Gabler1, Norbert Blank1, Joachim R. Kalden1, and Hanns-Martin Lorenz1

1 Department of Medicine III, Institute for Clinical Immunology and Rheumatology
2 Section of Endocrinology, Department of Medicine I, University of Erlangen-Nuremberg, 91054 Erlangen, Germany

Address correspondence to Martin A. Kriegel at his present address Section of Immunobiology, TAC S-560, Yale University School of Medicine, 300 Cedar St., P.O. Box 208011, New Haven, CT 06520. Phone: (203) 785-5383; Fax: (203) 737-2958; email: MartinKriegel{at}hotmail.com

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 (Tregs) 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. Tregs 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 Tregs 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.

Key Words: suppressor cells • autoimmune polyendocrinopathies • Addison's disease • type I diabetes • autoimmune thyroiditis


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