Differences in serum cytokine levels in acute and chronic autoimmune thrombocytopenic purpura: Relationship to platelet phenotype and antiplatelet T-cell reactivity
Differences in serum cytokine levels in acute and chronic autoimmune thrombocytopenic purpura: Relationship to platelet phenotype and antiplatelet T-cell reactivity
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DOI：
10.1182/blood.v87.10.4245.bloodjournal87104245
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发表时间：
1996-05-15
期刊：
影响因子：
20.3
通讯作者：
Freedman, J
中科院分区：
文献类型：
--
作者：
Semple, JW;Milev, Y;Freedman, J
急性和慢性自身免疫性血小板减少性紫癜（AITP）患者在体外都存在血小板刺激增殖和细胞因子分泌形式的淋巴细胞缺陷。进行盲法研究以确定这些缺陷是否与血清细胞因子水平和/或血小板抗原表达相关。与对照组相比，53%的慢性AITP患儿血清白细胞介素-2（IL-2）、干扰素-γ和/或IL-10水平升高，而急性AITP患儿仅为9%;然而，没有患者血清IL-4或IL-6水平可检测，细胞因子模式提示早期CD 4（+）Th 0和Th 1细胞活化。在慢性AITP儿童中，血清IL-2水平与体外血小板刺激的IL-2产生相关。少数（17%）AITP患者表现出血小板活化，如通过CD 62表达或血小板膜糖蛋白（GP）IIbIIIa的异常表达水平测量，但在三分之一的AITP儿童中观察到异常GPIb水平。与正常对照组和非免疫性血小板减少症患者相比，大量急性（80%）、慢性（71%）或慢性复合型（55%）AITP患儿外周血中GPIb（+）细胞表达HLA-DR。CD 45、CD 14、CD 80和/或血型糖蛋白分子。与对照组相比，从慢性AITP患者脾脏分离的GPIb（+）细胞具有高表达（49% +/- 30%）的HLA-DR，脾脏T细胞具有高水平的体外血小板刺激的IL-2分泌。血小板HLA-DR表达与血小板计数呈负相关，但与治疗、血清细胞因子或体外淋巴细胞抗血小板反应性无关。结果表明，血小板HLA-DR表达是一个常见的免疫性血小板减少症患者，而一个大的慢性AITP儿童亚群可以通过增加血清细胞因子水平和体外血小板刺激的IL-2分泌淋巴细胞，表明急性和慢性AITP的免疫发病机制存在差异，特别是在血小板反应性T细胞的水平。(C)1996年，美国血液学会。
Patients with both acute and chronic autoimmune thrombocytopenic purpura (AITP) have in vitro lymphocyte defects in the form of platelet-stimulated proliferation and cytokine secretion. A blinded study was performed to determine if these defects are related to serum cytokine levels and/or platelet antigen expression. Compared with controls, 53% of children with chronic AITP, but only 9% of those with acute AITP, had increased serum interleukin-2 (IL-2), interferon-gamma, and/or IL-10; however, none of the patients had detectible serum levels of IL-4 or IL-6, cytokine patterns suggesting an early CD4(+) Th0 and Th1 cell activation. In children with chronic AITP, the levels of serum IL-2 correlated with in vitro platelet-stimulated IL-2 production. Few (17%) patients with AITP showed platelet activation, as measured by CD62 expression, or abnormal expression levels of platelet membrane glycoprotein (GP) IIbIIIa, but abnormal GPIb levels were observed in one-third of children with AITP. In contrast to normal controls and patients with nonimmune thrombocytopenia, a significant number of children with acute (80%), chronic (71%), or chronic-complex (55%) AITP had GPIb(+) peripheral blood cells expressing HLA-DR. HLA-DR was variably coexpressed on distinct smaller and larger-sized GPIb(+) cell populations with CD41. CD45, CD14, CD80, and/or glycophorin molecules. GPIb(+) cells isolated from spleens of patients with chronic AITP had high expression (49% +/- 30%) of HLA-DR and splenic T cells had a high level of in vitro platelet-stimulated IL-2 secretion compared with controls. Platelet HLA-DR expression correlated inversely with platelet count, but not with therapy,serum cytokines, or in vitro lymphocyte antiplatelet reactivity. The results indicate that platelet HLA-DR expression is a common occurrence in patients with immune thrombocytopenia, whereas a large subpopulation of children with chronic AITP can be identified by increased serum cytokine levels and in vitro platelet-stimutated IL-2 secretion by lymphocytes, suggesting that differences exist in the immune pathogenesis of acute and chronic AITP, particularly at the level of platelet reactive T cells. (C) 1996 by The American Society of Hematology.