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小鼠T淋巴细胞表达血管活性肠肽受体1(VIP-R1)信使核糖核酸。

Murine T-lymphocytes express vasoactive intestinal peptide receptor 1 (VIP-R1) mRNA.

作者信息

Johnson M C, McCormack R J, Delgado M, Martinez C, Ganea D

机构信息

Department of Biological Sciences, Rutgers University, New York, NJ 07102, USA.

出版信息

J Neuroimmunol. 1996 Aug;68(1-2):109-19. doi: 10.1016/0165-5728(96)00085-9.

Abstract

Vasoactive intestinal peptide (VIP), a neuropeptide present in primary and secondary lymphoid organs has been previously reported to inhibit IL-2 and IL-4 production as well as the proliferation of mitogen- or antigen-stimulated T-cells. Binding studies suggested that the immunoregulatory effects of VIP are mediated through specific VIP-binding sites present on lymphocyte subpopulations. Here we report on the expression of VIP-R1 mRNA in various murine lymphocyte subpopulations. By using RT-PCR. RNase protection assay, cDNA cloning, and sequence analysis, we show that stimulated and unstimulated murine spleen cells, thymocytes. CD4+ and CD8+ T-cells express VIP-R1. The VIP-R1 fragment amplified from murine brain, thymocytes, spleen cells and CD4+ T-cells share identical nucleotide sequences, and a high degree of homology with the corresponding nonlymphoid rat and human VIP-R1 sequences. The expression of VIP-R1 in thymocytes and peripheral lymphocytes, and especially in the CD4+ T-cell subset supports the idea that VIP produced or released locally in the lymphoid microenvironment could directly affect cytokine production and proliferation of T-lymphocytes.

摘要

血管活性肠肽(VIP)是一种存在于初级和次级淋巴器官中的神经肽,此前有报道称它可抑制白细胞介素-2(IL-2)和白细胞介素-4(IL-4)的产生以及丝裂原或抗原刺激的T细胞增殖。结合研究表明,VIP的免疫调节作用是通过淋巴细胞亚群上存在的特定VIP结合位点介导的。在此,我们报告VIP-R1 mRNA在各种小鼠淋巴细胞亚群中的表达情况。通过使用逆转录聚合酶链反应(RT-PCR)、核糖核酸酶保护分析、cDNA克隆和序列分析,我们发现受刺激和未受刺激的小鼠脾细胞、胸腺细胞、CD4+和CD8+ T细胞均表达VIP-R1。从小鼠脑、胸腺细胞、脾细胞和CD4+ T细胞中扩增出的VIP-R1片段具有相同的核苷酸序列,并且与相应的非淋巴细胞大鼠和人类VIP-R1序列具有高度同源性。VIP-R1在胸腺细胞和外周淋巴细胞中,尤其是在CD4+ T细胞亚群中的表达支持了这样一种观点,即淋巴微环境中局部产生或释放的VIP可能直接影响T淋巴细胞的细胞因子产生和增殖。

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