Palecanda A, Briskin M J, Issekutz T B
Department of Medicine, University of Toronto, Ontario, Canada.
J Immunol. 1997 Mar 15;158(6):2904-10.
Mast cells are key mediators of allergy and inflammation. Increased mast cell numbers are observed in the gut during helminth infestation and at many sites of inflammation. To determine whether mast cells express functional receptors for endothelial cell adhesion molecules, we studied the adhesion of two rat mucosal-type mast cell lines RBL-1 and RCMC-1 to transfected mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and VCAM-1. Both mast cell lines expressed high levels of alpha4 integrins on their surface and bound to CHO cells transfected with VCAM-1. Anti-alpha4 mAbs, TA-2 and L25, inhibited the specific adhesion of the mast cells to VCAM-1 by about 92 and 63%, respectively. Both of the mast cell lines also demonstrated an increased adhesion to CHO cells transfected with MAdCAM-1. The adhesion of RBL-1 to MAdCAM-1 was also significantly inhibited by the anti-alpha4 mAbs TA-2, L25, and HP2/1 by 39, 76, and 42%, respectively. In addition, RBL-1 cells adhered to both VCAM-1 and MAdCAM-1 under both static and nonstatic (shear) conditions, and this was also inhibited by the anti-alpha4 mAb TA-2. Thus, mucosal-type mast cell lines express functional alpha4 integrins that can mediate adhesion to VCAM-1 and MAdCAM-1. These results suggest a mechanism for mast cell accumulation at sites of inflammation and in the gut.
肥大细胞是过敏和炎症的关键介质。在蠕虫感染期间以及许多炎症部位的肠道中，可观察到肥大细胞数量增加。为了确定肥大细胞是否表达内皮细胞黏附分子的功能性受体，我们研究了两种大鼠黏膜型肥大细胞系RBL-1和RCMC-1与转染的黏膜地址素细胞黏附分子-1（MAdCAM-1）和血管细胞黏附分子-1（VCAM-1）的黏附情况。两种肥大细胞系在其表面均高水平表达α4整合素，并与转染了VCAM-1的CHO细胞结合。抗α4单克隆抗体TA-2和L25分别抑制肥大细胞与VCAM-1的特异性黏附约92%和63%。两种肥大细胞系对转染了MAdCAM-1的CHO细胞的黏附也有所增加。抗α4单克隆抗体TA-2、L25和HP2/1分别使RBL-1与MAdCAM-1的黏附显著抑制39%、76%和42%。此外，RBL-1细胞在静态和非静态（剪切）条件下均能黏附于VCAM-1和MAdCAM-1，且这一过程也被抗α4单克隆抗体TA-2所抑制。因此，黏膜型肥大细胞系表达可介导与VCAM-1和MAdCAM-1黏附的功能性α4整合素。这些结果提示了肥大细胞在炎症部位和肠道中积聚的一种机制。
