Anti-CD43 inhibition of T cell homing.
Anti-CD43 inhibition of T cell homing.
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DOI：
10.1084/jem.185.8.1493
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发表时间：
1997-04-21
期刊：
影响因子：
--
通讯作者：
Butcher EC
中科院分区：
文献类型：
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作者：
McEvoy LM;Sun H;Frelinger JG;Butcher EC
淋巴细胞从血液中的归巢是由淋巴细胞-内皮细胞相互作用的特殊过程控制的。对这些过程的干扰提供了操纵淋巴细胞交通的可能性，从而调节正常和病理性免疫和炎症反应。我们选择抗淋巴细胞单克隆抗体（mab）来体外抑制淋巴细胞与淋巴结高内皮小静脉（HEV）的结合，HEV是支持淋巴细胞募集到淋巴结的特殊血管。mAb L11阻断T细胞与淋巴结和Peyer’s patch HEV的结合，并抑制T细胞从血液向有组织的次级淋巴组织外渗。相比之下，L11对淋巴细胞结合纯化血管配体的l -选择素、α4β7或LFA-1没有影响，表明它通过一种新机制抑制。L11抗原是CD43，一种唾液黏液蛋白，在体外参与淋巴细胞活化的调节，其表达在Wiskott-Aldrich综合征中经常失调。CD43代表了实验和治疗操作淋巴细胞运输的新靶点，可能有助于调节T细胞在体内的分布。
The homing of lymphocytes from the blood is controlled by specialized processes of lymphocyte–endothelial cell interaction. Interference with these processes offers the potential to manipulate lymphocyte traffic, and thus to modulate normal and pathologic immune and inflammatory responses. We selected antilymphocyte monoclonal antibodies (mAbs) for inhibition of lymphocyte binding in vitro to lymph node high endothelial venules (HEV), specialized vessels that support lymphocyte recruitment into lymph nodes. mAb L11 blocks T cell binding to lymph node and Peyer's patch HEV and inhibits T cell extravasation from the blood into organized secondary lymphoid tissues. In contrast, L11 has no effect on lymphocyte binding to purified vascular ligands for L-selectin, α4β7, or LFA-1, suggesting that it inhibits by a novel mechanism. The L11 antigen is CD43, a sialomucin implicated in vitro in regulation of lymphocyte activation, whose expression is often dysregulated in the Wiskott-Aldrich syndrome. CD43 represents a novel target for experimental and therapeutic manipulation of lymphocyte traffic and may help regulate T cell distribution in vivo.