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Blood, 15 August 2008, Vol. 112, No. 4, pp. 1325-1328.
Prepublished online as a Blood First Edition Paper on April 17, 2008; DOI 10.1182/blood-2008-01-135335.


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IMMUNOBIOLOGY

Brief Report

Defective circulating CD25 regulatory T cells in patients with chronic immune thrombocytopenic purpura

Jin Yu1,2,*, Susanne Heck3,*, Vivek Patel4, Jared Levan4, Yu Yu1, James B. Bussel4, and Karina Yazdanbakhsh1

1 Laboratory of Complement Biology, New York Blood Center, New York, NY; 2 Department of Integrative Medicine and Neurobiology, Shanghai Medical College, Fudan University, Shanghai, China; 3 Flow Cytometry Laboratory, New York Blood Center, New York, NY; and 4 Department of Pediatrics, Weill Medical College of Cornell University, New York, NY

Immune thrombocytopenic purpura (ITP) is characterized by the presence of antiplatelet autoantibodies as a result of loss of tolerance. CD4+CD25+ regulatory T cells (Tregs) are important for maintenance of peripheral tolerance. Decreased levels of peripheral Tregs in patients with ITP have been reported. To test whether inefficient production or reduced immunosuppressive activity of Tregs contributes to loss of tolerance in patients with chronic ITP, we investigated the frequency and function of their circulating CD4+CD25hi Tregs. We found a com-parable frequency of circulating CD4+CD25hiFoxp3+ Tregs in patients and controls (n = 16, P > .05). However, sorted CD4+CD25hi cells from patients with chronic ITP (n = 13) had a 2-fold reduction of in vitro immunosuppressive activity compared with controls (n = 10, P < .05). The impaired suppression was specific to Tregs as shown by cross-mixing experiments with T cells from controls. These data suggest that functional defects in Tregs contribute to breakdown of self-tolerance in patients with chronic ITP.


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