Role of vascular cell adhesion molecule 1/very late activation antigen 4 and intercellular adhesion molecule 1/lymphocyte function-associated antigen 1 interactions in antigen-induced eosinophil and T cell recruitment into the tissue.
Role of vascular cell adhesion molecule 1/very late activation antigen 4 and intercellular adhesion molecule 1/lymphocyte function-associated antigen 1 interactions in antigen-induced eosinophil and T cell recruitment into the tissue.
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DOI：
10.1084/jem.179.4.1145
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发表时间：
1994-04-01
期刊：
影响因子：
--
通讯作者：
Iwamoto I
中科院分区：
文献类型：
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作者：
Nakajima H;Sano H;Nishimura T;Yoshida S;Iwamoto I
为了确定血管细胞粘附分子 1 (VCAM-1)/极晚期活化抗原 4 (VLA-4) 和细胞间粘附分子 1 (ICAM-1)/淋巴细胞功能相关抗原 1 (LFA-1) 相互作用在引起抗原诱导的嗜酸性粒细胞和 T 细胞募集到组织中的作用，我们研究了体内阻断的效果 通过用针对这四种粘附分子的单克隆抗体（mAb）预处理，研究VCAM-1、ICAM-1、VLA-4和LFA-1对小鼠抗原吸入诱导的气管嗜酸性粒细胞和T细胞浸润的影响。体内阻断VCAM-1和VLA-4，但不阻断ICAM-1和LFA-1，可以防止抗原诱导的嗜酸性粒细胞浸润到小鼠气管中。相反，在致敏小鼠中，体内阻断VCAM-1和VLA-4，但不阻断ICAM-1和LFA-1，增加了抗原攻击后的血液嗜酸性粒细胞计数，但不影响未经抗原攻击的血液嗜酸性粒细胞计数。此外，抗原攻击后，气管内皮上强烈诱导VCAM-1而非ICAM-1的表达。此外，用抗IL-4 mAb预处理仅使抗原诱导的VCAM-1表达降低27%，并且对抗原诱导的嗜酸性粒细胞浸润气管没有显着影响。体内阻断 VCAM-1 和 VLA-4 比 ICAM-1 和 LFA-1 更有效地抑制抗原诱导的 CD4+ 和 CD8+ T 细胞浸润气管。相反，无论抗原攻击如何，体内阻断 LFA-1（而非 ICAM-1）比 VCAM-1 和 VLA-4 增加的血液淋巴细胞计数更多。这些结果表明，VCAM-1/VLA-4 相互作用在控制抗原诱导的嗜酸性粒细胞和 T 细胞募集到组织中起主要作用，并且诱导过敏性炎症部位内皮上的 VCAM-1 表达可调节这种嗜酸性粒细胞和 T 细胞募集。
To determine the role of vascular cell adhesion molecule 1 (VCAM- 1)/very late activation antigen 4 (VLA-4) and intercellular adhesion molecule 1 (ICAM-1)/lymphocyte function-associated antigen 1 (LFA-1) interactions in causing antigen-induced eosinophil and T cell recruitment into the tissue, we studied the effect of the in vivo blocking of VCAM-1, ICAM-1, VLA-4, and LFA-1 by pretreatment with monoclonal antibodies (mAb) to these four adhesion molecules on the eosinophil and T cell infiltration of the trachea induced by antigen inhalation in mice. The in vivo blocking of VCAM-1 and VLA-4, but not of ICAM-1 and LFA-1, prevented antigen-induced eosinophil infiltration into the mouse trachea. On the contrary, the in vivo blocking of VCAM-1 and VLA-4, but not of ICAM-1 and LFA-1, increased blood eosinophil counts after antigen challenge, but did not affect blood eosinophil counts without antigen challenge in sensitized mice. Furthermore, the expression of VCAM-1 but not ICAM-1 was strongly induced on the endothelium of the trachea after antigen challenge. In addition, pretreatment with anti-IL-4 mAb decreased the antigen-induced VCAM-1 expression only by 27% and had no significant effect on antigen-induced eosinophil infiltration into the trachea. The in vivo blocking of VCAM- 1 and VLA-4 inhibited antigen-induced CD4+ and CD8+ T cell infiltration into the trachea more potently than that of ICAM-1 and LFA-1. In contrast, regardless of antigen challenge, the in vivo blocking of LFA- 1, but not of ICAM-1, increased blood lymphocyte counts more than that of VCAM-1 and VLA-4. These results indicate that VCAM-1/VLA-4 interaction plays a predominant role in controlling antigen-induced eosinophil and T cell recruitment into the tissue and that the induction of VCAM-1 expression on the endothelium at the site of allergic inflammation regulates this eosinophil and T cell recruitment.