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血管活性肠肽通过可能涉及蛋白激酶C的机制增强人浆细胞中的免疫球蛋白产生和生长。

Vasoactive intestinal peptide enhances immunoglobulin production and growth in human plasma cells via mechanisms that may involve protein kinase C.

作者信息

Kimata H, Yoshida A, Ishioka C, Fujimoto M, Furusho K

机构信息

Department of Pediatrics, Unitika Central Hospital, Uji, Japan.

出版信息

J Clin Endocrinol Metab. 1996 Aug;81(8):3024-32. doi: 10.1210/jcem.81.8.8768869.

DOI:10.1210/jcem.81.8.8768869
PMID:8768869
Abstract

The effects of various neuropeptides on human plasma cells were studied. Of the various neuropeptides tested, vasoactive intestinal peptide (VIP) enhanced Ig production and growth in human plasma cell lines, IM-9 and AF-10, and in plasma cells generated in vivo (four out of four patients with plasma cell leukemia) and in vitro. In contrast, other neuropeptides (neuropeptide Y, somatostatin, substance P, peptide YY, neurokinin A, calcitonin gene-related peptide, chole-cystokinin octapeptide, and beta-endorphin) were ineffective. Moreover, VIP-induced enhancement was specifically blocked by VIP receptor antagonist. Among the various cytokines, IL-6, GH, and insulin-like growth factor I (IGF-I) also enhanced Ig production and thymidine uptake in plasma cells. However, VIP-induced enhancement was not mediated by IL-6, GH, or IGF-I because antibodies to these cytokines failed to block VIP-induced enhancement. Phorbol 12,13 dibutyrate enhanced Ig production and thymidine uptake in plasma cells, and the Phorbol 12,13 dibutyrate-induced enhancement was blocked by H7 (a protein kinase C inhibitor) but not by H8 (a protein kinase A inhibitor). Similarly, VIP-induced enhancement was blocked by H7 but not by H8. Collectively, VIP enhances plasma cell responses via mechanisms that may involve protein kinase C.

摘要

研究了各种神经肽对人浆细胞的影响。在测试的各种神经肽中,血管活性肠肽(VIP)可增强人浆细胞系IM-9和AF-10以及体内产生的浆细胞(4例浆细胞白血病患者中的4例)和体外产生的浆细胞中的Ig产生和生长。相比之下,其他神经肽(神经肽Y、生长抑素、P物质、肽YY、神经激肽A、降钙素基因相关肽、胆囊收缩素八肽和β-内啡肽)则无效。此外,VIP受体拮抗剂可特异性阻断VIP诱导的增强作用。在各种细胞因子中,IL-6、生长激素(GH)和胰岛素样生长因子I(IGF-I)也可增强浆细胞中的Ig产生和胸苷摄取。然而,VIP诱导的增强作用不是由IL-6、GH或IGF-I介导的,因为针对这些细胞因子的抗体未能阻断VIP诱导的增强作用。佛波酯12,13 -二丁酸酯可增强浆细胞中的Ig产生和胸苷摄取,且佛波酯12,13 -二丁酸酯诱导的增强作用可被H7(一种蛋白激酶C抑制剂)阻断,但不能被H8(一种蛋白激酶A抑制剂)阻断。同样,VIP诱导的增强作用可被H7阻断,但不能被H8阻断。总体而言,VIP通过可能涉及蛋白激酶C的机制增强浆细胞反应。

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