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Prepublished online as a Blood First Edition Paper on November 21, 2002; DOI 10.1182/blood-2002-06-1666.
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Blood, 1 April 2003, Vol. 101, No. 7, pp. 2721-2726
IMMUNOBIOLOGY
Effects of B7-blocking agent and/or CsA on induction of
platelet-specific T-cell anergy in chronic autoimmune thrombocytopenic
purpura
Jun Peng,
Chuanfang Liu,
Dai Liu,
Cuiai Ren,
Wei Li,
Zhenguang Wang,
Nianzeng Xing,
Conggao Xu,
Xueliang Chen,
Chunyan Ji,
Maohong Zhang, and
Ming Hou
From the Department of Hematology, and the Department
of Nuclear Medicine, Qilu Hospital of Shandong University; the
Department of Science and Technology, Shandong University, Jinan,
Shandong, People's Republic of China; the Department of
Hematology, People's Hospital, Weifang, Shandong, People's
Republic of China; the Department of Hematology, Affiliated
Hospital of Medical College of Qingdao University, Qingdao, Shandong,
People's Republic of China; and the Department of
Urology, Beijing Chao Yang Hospital affiliated to Capital University of
Medical Sciences, Beijing, People's Republic of China.
Chronic autoimmune thrombocytopenic purpura (AITP) is characterized
by platelet-specific autoantibody production that is influenced by
enhanced antiplatelet T-helper cell reactivity. Costimulatory signals
are absolutely required for T-cell activation and play key roles in the
decision between tolerance and immunity. In this study we cultured T
cells isolated from patients with chronic AITP to investigate the
effects of the B7-blocking agent cytologic T-lymphocyte-associated
antigen 4-immunoglobulin (CTLA4-Ig), and cyclosporin A (CsA),
alone or in combination, on induction of platelet-specific T-cell
anergy. The data showed that in most cases CTLA4-Ig and/or CsA could
induce tolerance toward platelet antigens based on anergy. It could be
overcome by stimulation with unrelated antigens, demonstrating its
platelet specificity. The anergy is associated with lack of interleukin
2 (IL-2) and withheld by exogenous IL-2, emphasizing the
pivotal role of IL-2 suppression in the induction of platelet-specific
anergy. We also prospectively evaluated the efficacy of CsA therapy in
patients with refractory AITP and observed that the response to CsA
treatment in vivo was associated with the inhibiting sensitivity of
platelet-reactive T cells to CsA in vitro. This suggests that the
sensitivity of T cells to CsA in vitro could serve as a reliable
parameter in predicting the efficacy of CsA for patients with
refractory AITP. CTLA4-Ig may become a promising new therapeutic agent
for the treatment of chronic AITP, and the combination of CTLA4-Ig and CsA would be a more powerful strategy for the management of refractory AITP.
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