Blum A M, Mathew R, Cook G A, Metwali A, Felman R, Weinstock J V
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
J Neuroimmunol. 1992 Jul;39(1-2):101-8. doi: 10.1016/0165-5728(92)90179-o.
Reports suggest that vasoactive intestinal peptide (VIP) binds to lymphocytes and modulates immune responses. The intestines are richly innervated with VIP-producing nerves. Thus, VIP from nerves or other sources may participate in mucosal immunoregulation. To explore this hypothesis further, murine intestinal mucosal inflammatory cells were scrutinized for functional VIP receptors. An [125I]VIP competitive binding assay characterized VIP receptors. Unfractionated lamina propria inflammatory cells bound [125I]VIP specifically. This binding was abrogated by T cell depletion. The VIP receptor on lamina propria T cells was of a single class with a Kd of 9.08 x 10(-9) M. It bound PHI and other peptide analogs poorly. The intestinal epithelial cell had a high-affinity VIP receptor (Kd 4.17 x 10(-10) M) that bound one VIP analog with moderate affinity. Both VIP and ConA stimulated mucosal inflammatory cells to release interleukin-5 (IL-5). Mucosal inflammatory cells depleted of T cells did not release IL-5 in response to VIP or ConA. It is concluded that: (1) some murine mucosal T lymphocytes have VIP receptors that may be distinct from those displayed on mucosal epithelial cells; (2) VIP affects mucosal T lymphocyte function.
报告表明，血管活性肠肽（VIP）与淋巴细胞结合并调节免疫反应。肠道富含产生VIP的神经支配。因此，来自神经或其他来源的VIP可能参与黏膜免疫调节。为了进一步探究这一假说，对小鼠肠道黏膜炎症细胞进行了功能性VIP受体的仔细研究。采用[125I]VIP竞争性结合试验对VIP受体进行了表征。未分级的固有层炎症细胞特异性结合[125I]VIP。这种结合因T细胞耗竭而消除。固有层T细胞上的VIP受体为单一类型，解离常数（Kd）为9.08×10^(-9)M。它与PHI和其他肽类似物结合较差。肠上皮细胞有一个高亲和力的VIP受体（Kd 4.17×10^(-10)M），该受体以中等亲和力结合一种VIP类似物。VIP和刀豆蛋白A（ConA）均刺激黏膜炎症细胞释放白细胞介素-5（IL-5）。去除T细胞的黏膜炎症细胞对VIP或ConA无反应，不释放IL-5。结论如下：（1）一些小鼠黏膜T淋巴细胞具有VIP受体，这些受体可能与黏膜上皮细胞上的受体不同；（2）VIP影响黏膜T淋巴细胞功能。
