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白细胞介素(IL)-13而非IL-4参与肾病综合征中自发性IgE和IgG4的产生。

Involvement of interleukin (IL)-13, but not IL-4, in spontaneous IgE and IgG4 production in nephrotic syndrome.

作者信息

Kimata H, Fujimoto M, Furusho K

机构信息

Department of Pediatrics, Kyoto University Hospital, Japan.

出版信息

Eur J Immunol. 1995 Jun;25(6):1497-501. doi: 10.1002/eji.1830250604.

Abstract

Nephrotic syndrome (NS) is a renal disease characterized by proteinuria and hypoalbuminemia. In NS patients without any allergic disease, serum IgE and IgG4 levels were selectively increased, and peripheral blood mononuclear cells (MNC) spontaneously produced IgE and IgG4. T cells produced interleukin (IL)-13 spontaneously, and B cells constitutively expressed IL-13 receptors (IL-13R). In addition, T cells stimulated surface IgE-negative (sIgE-) and sIgG4- B cells to produce IgE and IgG4, respectively, and IgE and IgG4 production was specifically blocked by anti-IL-13 antibody (Ab). MNC from atopic dermatitis (AD) patients also produced IgE and IgG4 spontaneously. However, in AD patients, T cells spontaneously produced IL-4, but not IL-13, and B cells constitutively expressed IL-4R, but not IL-13R. T cells stimulated sIgE- and sIgG4- B cells to produce IgE and IgG4, respectively, and the production was specifically blocked by anti-IL-4 Ab. On the other hand, sIgE+ and sIgG4+ B cells from both NS and AD patients spontaneously produced IgE and IgG4, respectively, and this production was not affected by T cells, anti-IL-4 Ab, or anti-IL-13 Ab. These results indicate that IL-13 is involved in the enhanced production of IgE and IgG4 in NS, while IL-4 is involved in these responses in AD.

摘要

肾病综合征(NS)是一种以蛋白尿和低白蛋白血症为特征的肾脏疾病。在没有任何过敏性疾病的NS患者中,血清IgE和IgG4水平选择性升高,外周血单个核细胞(MNC)可自发产生IgE和IgG4。T细胞可自发产生白细胞介素(IL)-13,B细胞组成性表达IL-13受体(IL-13R)。此外,T细胞刺激表面IgE阴性(sIgE-)和sIgG4- B细胞分别产生IgE和IgG4,且IgE和IgG4的产生可被抗IL-13抗体(Ab)特异性阻断。特应性皮炎(AD)患者的MNC也可自发产生IgE和IgG4。然而,在AD患者中,T细胞自发产生IL-4而非IL-13,B细胞组成性表达IL-4R而非IL-13R。T细胞刺激sIgE-和sIgG4- B细胞分别产生IgE和IgG4,且该产生可被抗IL-4 Ab特异性阻断。另一方面,NS和AD患者的sIgE+和sIgG4+ B细胞分别可自发产生IgE和IgG4,且该产生不受T细胞、抗IL-4 Ab或抗IL-13 Ab的影响。这些结果表明,IL-13参与了NS中IgE和IgG4的增强产生,而IL-4参与了AD中的这些反应。

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