Elevations in IFN-gamma, IL-5, and IL-10 in patients with the autoimmune disease primary biliary cirrhosis: Association with autoantibodies and soluble CD30
Elevations in IFN-gamma, IL-5, and IL-10 in patients with the autoimmune disease primary biliary cirrhosis: Association with autoantibodies and soluble CD30
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DOI：
10.1006/clin.1996.0129
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发表时间：
1996-09-01
期刊：
影响因子：
--
通讯作者：
Martinez, OM
中科院分区：
文献类型：
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作者：
Krams, SM;Cao, S;Martinez, OM
抗线粒体抗体（AMA），识别丙酮酸脱氢酶复合物的E2组分，发现在几乎所有的自身免疫性肝病原发性胆汁性肝硬化（PBC）患者。导致AMA升高的因素以及自身抗体与疾病发病机制的关系尚未阐明。由于细胞因子是抗体产生和同种型转换的重要调节因子，因此在PBC患者中检查了特异性细胞因子与抗体产生的关联。在PBC患者血清中检测到IL-2、IFN-γ、IL-4、IL-5和IL-10的升高。然而，与正常对照组相比，只有IFN-γ（6012 +/- 1128 pg/ml vs 147 +/- 89 pg/ml，P < 0.0001）和IL-5（382 +/- 103 pg/ml vs 29 +/- 12 pg/ml，P < 0.001）显著升高。此外，IFN-γ水平与循环中可溶性CD 30（sCD 30）水平呈正相关，IL-5水平次之。PBC患者血清sCD 30水平明显升高（194 ± 29 U/ml vs 39 ± 9 U/ml），提示PBC患者外周血中CD 30（+）细胞可能产生细胞因子，参与PBC患者的免疫异常。(C)中国科学院出版社
Antimitochondrial antibodies (AMA) which recognize the E2 component of the pyruvate dehydrogenase complex are found in virtually all patients with the autoimmune liver disease primary biliary cirrhosis (PBC). The factors that contribute to elevated AMA and the relationship of the autoantibodies to disease pathogenesis have not been elucidated. Since cytokines are important regulators of antibody production and isotype switching, the association of specific cytokines to antibody production was examined in patients with PBC. Elevations in IL-2, IFN-gamma, IL-4, IL-5, and IL-10 were detected in serum from patients with PBC. However, only IFN-gamma (6012 +/- 1128 pg/ml vs 147 +/- 89 pg/ml, P < 0.0001) and IL-5 (382 +/- 103 pg/ml vs 29 +/- 12 pg/ml, P < 0.001) were significantly elevated compared to normal controls. Moreover, there was a positive correlation in the levels of IFN-gamma, and to a lesser extent IL-5, with the levels of soluble CD30 (sCD30) in the circulation. The elevated levels of sCD30 detected in patients with PBC (194 + 29 U/ml vs 39 +/- 9 U/ml in normal controls) suggest that CD30(+) cells may produce cytokines, which contribute to the immune abnormalities in patients with PBC. (C) 1996 Academia Press, Inc.