Goetzl E J, Pankhaniya R R, Gaufo G O, Mu Y, Xia M, Sreedharan S P
Department of Medicine, University of California Medical Center, San Francisco 94143, USA.
Ann N Y Acad Sci. 1998 May 1;840:540-50. doi: 10.1111/j.1749-6632.1998.tb09593.x.
The major immunoregulatory effects of vasoactive intestinal peptide (VIP) are mediated by structurally distinct type I (VIPR1) and II (VIPR2) G protein-associated receptors on many different types of immune cells. VIP is released in functionally relevant concentrations during many immunologic and inflammatory responses. Mast cells (VIPR1), macrophages (VIPR1 and VIPR2), B cells, and T cells (VIPR1, VIPR2, or VIPR1 and VIPR2) recognize and respond to VIP in patterns that are controlled by the relative levels of expression of VIPR1 and VIPR2. VIPR2 transduces human T-cell chemotaxis, expression of matrix metalloproteinases (MMPs) 2 and 9 and consequently basement membrane and connective tissue transmigration, while signaling suppression of proliferation and cytokine production. In contrast, VIPR1 fails to transduce T-cell chemotaxis but mediates suppression of chemotaxis and MMP expression elicited by some cytokines and chemokines. The relative representation of each type of VIPR, which is presumed to be under cytokine control, thus may determine T-cell responses to VIP and other immune mediators in tissue compartments innervated by VIPergic nerves.
血管活性肠肽（VIP）的主要免疫调节作用是由许多不同类型免疫细胞上结构不同的I型（VIPR1）和II型（VIPR2）G蛋白偶联受体介导的。在许多免疫和炎症反应过程中，VIP以功能相关的浓度释放。肥大细胞（VIPR1）、巨噬细胞（VIPR1和VIPR2）、B细胞和T细胞（VIPR1、VIPR2或VIPR1和VIPR2）以受VIPR1和VIPR2相对表达水平控制的模式识别并对VIP作出反应。VIPR2介导人T细胞趋化、基质金属蛋白酶（MMP）2和9的表达，进而介导基底膜和结缔组织迁移，同时抑制增殖和细胞因子产生的信号传导。相比之下，VIPR1不能介导T细胞趋化，但能介导对某些细胞因子和趋化因子引发的趋化和MMP表达的抑制。每种类型VIPR的相对表达情况（推测受细胞因子控制）可能决定T细胞对VIP和其他免疫介质在由VIP能神经支配的组织区域中的反应。
