Leptin enhances in vitro secretion of IgG antiplatelet antibodies by splenocytes and peripheral blood mononuclear cells from patients with chronic idiopathic thrombocytopenic purpura

被引:30
作者
Ren, He
Zhao, Hui
Wang, Tingting
Yang, Yanhui
Han, Zhibo
Liu, Bin
Wu, Zida
Tao, Jie
Zhou, Bin
Zhang, Lei
Yang, Renchi [1 ]
Han, Zhong Chao
机构
[1] Chinese Acad Med Sci, Inst Hematol, State Key Lab Expt Hematol, Tianjin 300020, Peoples R China
[2] Peking Univ, Coll Med, Tianjin 300020, Peoples R China
[3] Univ Med Berlin, Dept Med 4, Div Clin Endocrinol, Res Labs, Berlin, Germany
关键词
chronic idiopathic thrombocytopenic pupura; leptin; leptin receptor; splenocytes; peripheral blood mononuclear cells; antiplatelet antibodies;
D O I
10.1016/j.clim.2006.04.573
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
Chronic idiopathic thrombocytopenic purpura (ITP) is an organ-specific autoimmune disease characterized by the production of antibodies against antigens on the membranes of platelets, resulting in enhanced destruction of the platelets by macrophages. Leptin, a cytokine-like hormone, plays a role in the pathogenesis of several autoimmune diseases. In this study, we observed significantly increased plasma leptin levels combined with decreased soluble leptin receptor (sOB-R) levels in 18 chronic ITP patients compared with 14 controls. We also demonstrated significantly elevated mRNA expression of long form leptin receptor (Ob-Rb) on peripheral blood mononuclear cells (PBMCs) from chronic ITP patients. Treatment with recombinant leptin or serum with high leptin levels enhanced in vitro secretion of IgG antiplatetet antibodies by splenocytes and PBMCs from patients with chronic ITR. After depletion of CD4(+) T cells from splenocytes, leptin lost this function. Further studies showed that Leptin could increase platelet reactive Tcells. These findings suggest that leptin may be involved in the pathogenesis of chronic ITP and might offer a potential target for the treatment of this disease. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:205 / 211
页数:7
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