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Analysis of adhesion molecules on mast cells

肥大细胞上粘附分子的分析

基本信息

批准号：
05044187
负责人：
HIRANO Takao
金额：
$ 3.46万
依托单位：
Juntendo University
依托单位国家：
日本
项目类别：
Grant-in-Aid for international Scientific Research
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1995
项目状态：
已结题

项目摘要

Adhesion molecules of the integrin family are implicated not only in leukocyte migration but also in leukocyte activation. Here we characterize the expression and function of fibronectin receptor integrins on rat mast cells. A rat basophilic leukemia cell line (RBL-2H3) and phorbol ester-stimulated rat peritoneal mast cells adhered to fibronectin (FN), vitronectin and fibrinogen. These mast cells expressed fibronectin receptor integrins, including very late antigen (VLA)-4, VLA-5 and virtonectin receptor (VNR), as estimated by immunofluorescent staining and inhibition of FN adherence by newly established mAbs reactive with the rat alpha4 (MRalpha4-1), alpha5 (HMalpha5-1) or beta3 (HMbeta3-1) chains of the integrin molecules. The beta-hexosaminidase release, a marker for mast cell degranulation, triggered by high affinity IgE receptor (FcepsilonRI) -mediated stimulation, was enhanced by adhesion of RBL-2H3 cells to either immunobilized FN,MRalpha4-1, HMalpha5-1, or HMbeta3-1. This FN enhancement of beta-hexosaminidase release was inhibited by soluble MRalpha4-1, H M alpha5-1, and HMbeta3-1 as well as by GRGDSP and DELPQLVTLPHPNHLGPEILDVPST peptides which abrogate VLA-5/VNR and VLA-4 binding to FN respectively. In vivo, passive cutaneous anaphylaxis induced by IgE anti-DNP and DNP-BSA was inhibited by concurrent s.c. injection of MRalpha4-1, HMalpha5-1, and HMbeta3-1. These results demonstrate that FN receptor integrins expressed on rat mast cells play an important role in regulating mast cell activation both in vitro and in in vivo.

整合素家族的粘附分子不仅参与白细胞迁移，而且参与白细胞活化。在这里，我们的特点的表达和功能的纤维连接蛋白受体整合素对大鼠肥大细胞。大鼠嗜碱性白血病细胞系（RBL-2 H3）和佛波酯刺激的大鼠腹腔肥大细胞粘附纤维连接蛋白（FN），玻连蛋白和纤维蛋白原。这些肥大细胞表达纤连蛋白受体整合素，包括极晚期抗原（VLA）-4，VLA-5和virtonectin受体（VNR），如通过免疫荧光染色和新建立的与大鼠整合素分子的α 4（MR α 4 -1），α 5（HM α 5 -1）或β 3（HM β 3 -1）链反应的mAb对FN粘附的抑制所估计的。β-氨基己糖苷酶的释放是肥大细胞脱粒的标志物，由高亲和力IgE受体（Fc ε RI）介导的刺激触发，通过RBL-2 H3细胞粘附于免疫活化的FN、MR α 4 -1、HMalpha 5 -1或HM β 3 -1而增强。这种FN对β-氨基己糖苷酶释放的增强作用受到可溶性MR α 4 -1、HM α 5 -1和HM β 3 -1以及GRGDSP和DELPQLVTLPHPNHLGPEILDVPST肽的抑制，所述肽分别消除VLA-5/VNR和VLA-4与FN的结合。在体内，由IgE抗DNP和DNP-BSA诱导的被动皮肤过敏反应被同时s.c.注射MR α 4 -1、HM α 5 -1和HM β 3 -1。这些结果表明，大鼠肥大细胞上表达的FN受体整合素在调节肥大细胞活化中起重要作用，在体外和体内。