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

Yu J, Heck S, Patel V +4 more2008BloodJournal Article
HematologicalImmune/Innate

Abstract

From bloodjournal.hematologylibrary.or~ by guest on February 29, 2012. For personal use orlly. IMMUNOBIOLOGY Defective circulating CD25 regulatory T cells in patients with chronic immune thrombocytopenic purpura "Jin YU,'.~ "Susanne Heck,3 Vivek Patel,4 Jared L e ~ a n , ~ and Karina Yazdanbakhshl Yu Yu,' James B. B ~ s s e l , ~ 'Laboratory of Complement Biology, New York Blood Center, New York, NY; >Department of Integrative Medicine and Neurobiology, Shanghai Medical College, Fudan University, Shanghai, China; Flow Cytometry Laboratory, New York Blood Center, New York, NY; and 4Department of Pedlatrics. Weill Medical College crf Cornell University, New York. NY Immune thrombocytopenic purpura (ITP) to loss of tolerance in patients with activity compared with controls (n = 10, is characterized by the presence of anti- chronic ITP, we investigated the fre- P i .05). The impaired suppression was platelet autoantibodies as a result of loss quency and function of their circulating specific to Tregs as shown by cross- of tolerance. CD4+CD25+ regulatory CD4+CD25hi Tregs. We found a corn- mixing experiments with T cells from con- T cells (Tregs) are important for mainte- parable frequency of circulating trols. These data suggest that functional nance of peripheral tolerance. Decreased CD4+CD25hiFoxp3+ Tregs in patients and defects in Tregs contribute to breakdown levels of peripheral Tregs in patients with controls (n = 16, P > .05). However, of self-tolerance in patients with chronic ITP have been reported. To test whether sorted CD4+CD25hi cells from patients ITP. (Blood. 2008;112:1325-1328) inefficient production or reduced irnmuno- with chronic ITP (n = 13) had a 2-fold suppressive activity of Tregs contributes reduction of in vitro immunosuppressive Introduction lmmu~ie thrombacylopenic purpllra (ITP) is a bleeding disorder characterized by production of autoreactive antibodies to platelet i~ntigens, resulting in both accelerated destruction of platelets and reduced

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Key Biomarkers

Anti-platelet autoantibodiesTregs

Symptom Clusters

Autoimmune responseLoss of toleranceThrombocytopenia