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Blood, 1 May 2005, Vol. 105, No. 9, pp. 3746-3748.
Prepublished online as a Blood First Edition Paper on January 6, 2005; DOI 10.1182/blood-2004-12-4692.
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Submitted December 9, 2004
Accepted December 27, 2004
CD4+CD25+ regulatory T cells control induction of autoimmune hemolytic anemia
Amina Mqadmi, Xiaoying Zheng, and Karina Yazdanbakhsh*
Complement Biology, New York Blood Center, New York, NY, USA
* Corresponding author; email: kyazdanbakhsh{at}nybloodcenter.org.
Autoimmune hemolytic anemia (AIHA) is the result of increased destruction of red blood cells (RBCs) due to the production of autoantibodies and can be life-threatening. To study mechanisms that trigger AIHA, we used the Marshall-Clarke and Playfair model of murine AIHA, in which mice repeatedly immunized with rat RBCs develop erythrocyte autoantibodies as well as rat-specific alloantibodies. We analyzed the role of CD25+ T regulatory subsets in controlling AIHA in C57/Bl6 mice using antibody depletion studies. Treatment with anti-CD25 antibody, but not isotype control prior to immunization with rat RBCs increased the incidence of AIHA from 30% to 90%. Adoptive transfer of purified splenic population of CD4+CD25+, but not CD4+CD25- cells from immunized mice into naive recipients prevented the induction of autoantibody production. Altogether, our data establishes a critical role for CD4+CD25+ cells for control of AIHA which may help to establish therapeutic strategies for treatment of AIHA.

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