Immunological Analysis and Regulation of Platelet Activation in Delayed-Type Hypersensitivity

Platelets Express特定的接受器，如IgE和粘合剂分子和激活机制，通过他们被证明是正确的。在目前的研究项目中，我们调查了在延迟型高敏感性、接触敏感性和大气性皮肤病过程中可能的参与。已获得的结果将继续：1）与BA Yu 3405的活体治疗（thromboxane A型D22型D2） TXA型D22型D2受体拮抗剂， markedly suppressed CS responses in genetically most cell-deficient W/W型D1 vieD 1型老鼠和抑制剂效应被occurred when BA Yu 3405在早期启动期之前被管理，建议TXA-D22-D2可能是平台介导的CS响应的潜在启动器。2）当平台被BA Yu 3405在体外、平台聚合作为血清素释放良好时，什么是有可能诱导早期阶段的反应允许CS效应器T细胞的局部反应，以便直接激活血管内容细胞，Furthermore，U46619的补充，TXA-D22-D2的拮抗剂，或两种改进的ICAM-1和VCAM-1在隔离小鼠星形内皮细胞上表达的平台和血栓的混合，完全被BA Yu 3405预先处理。这些发现建议从TXA-D22-D2生成的平台激活的Ag可能介导启动的CS响应，从而导致从平台释放的血清素及其亚序列聚合和升级表达的ICAM-1和VCAM-1上的血管内内皮细胞. 4）在激活的平台的膜上表达的左旋磷脂酰丝氨酸是可能的-介神经增长因子。血清素形成大鼠Peritoneal Mast Cells的相关释放。这一淋巴细胞系介导的细胞激活在体内被证实，并在过敏反应中提供了一个新颖的证据，在炎症反应中提供了一个炎症级联。

Platelets express specific receptors such as IgE and adhesion molecules and activation mechanisms through them have been discussed. In the present research project, we investigated the possible involvement of platelets in the process of delayed-type hypersensitivity, such as contact sensitivity and atopic dermatitis. The obtained resulted are follows:1) In vivo treatment with BA Yu3405, a (thromboxane AィイD22ィエD2) TXAィイD22ィエD2 receptor antagonist, markedly suppressed CS responses in genetically mast cell-deficient W/WィイD1vィエD1 mice and the inhibitory effect was occurred when BA Yu3405 was administered before an early initiating phase, suggesting that TXAィイD22ィエD2 may be a potent initiator of platelet-mediated CS responses.2) When platelets were pretreated with BA Yu3405 in vitro, platelet aggregation as well as serotonin release, which is able to induce the early phase response allowing local recruitment of CS effector T cells due to direct activation of vascular endothelial cells, was inhibited.3) Furthermore, the addition of U46619, a TXAィイD22ィエD2 agonist, or mixture of platelets and thrombin enhanced expression of both ICAM-1 and VCAM-1 on isolated mouse aortic endothelial cells, which was completely abolished by the pretreatment with BA Yu3405. These findings suggest that TXAィイD22ィエD2 generated from platelets activated with Ag may mediate initiation of CS responses through leading serotonin release from platelets and the subsequent aggregation and upregulating expression of ICAM-1 and VCAM-1 on the vascular endothelial cells.4) Lysophosphatidylserine expressed on the membrane of the activated platelets was able to mediate nerve growth factor-dependent release of serotonin form rat peritoneal mast cells. This lysophosphatidylserine-mediated mast cell activation was demonstrated in vivo, providing novel evidence of an inflammatory cascade in allergic responses.