T cell-dependent mast cell degranulation and release of serotonin in murine delayed-type hypersensitivity.
T cell-dependent mast cell degranulation and release of serotonin in murine delayed-type hypersensitivity.
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DOI：
10.1084/jem.152.5.1358
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发表时间：
1980-11-01
期刊：
影响因子：
--
通讯作者：
Gershon RK
中科院分区：
文献类型：
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作者：
Askenase PW;Bursztajn S;Gershon MD;Gershon RK
我们先前已经提出，局部组织肥大细胞释放5-羟色胺(5-羟色胺)是诱发小鼠迟发型超敏反应(DTH)所必需的。在本研究中，经[~3H]5-HT处理的动物的光镜放射自显影表明，在DTH的演变过程中，局部肥大细胞在6~18h之间释放了5-HT。超微结构检查显示肥大细胞表面活化，表面丝状足突伸展，融合和胞吐脱颗粒。对DTH部位毛细血管后小静脉内皮细胞的光镜和电子显微镜观察显示，相邻细胞之间有间隙的形成。间隙的形成允许示踪剂的外溢，而示踪剂因5-羟色胺的耗尽或拮抗而被消除。在DTH中，肥大细胞脱颗粒并释放5-羟色胺，5-羟色胺作用于局部血管。非粘附性、非免疫球蛋白致敏淋巴细胞的受者也表现出类似的肥大细胞脱颗粒和内皮间隙的形成。提示小鼠迟发型超敏反应中肥大细胞脱颗粒和5-羟色胺的释放可能是T细胞依赖性的。
We have previously suggested that the release of serotonin (5- hydroxytryptamine) (5-HT) by local tissue mast cells is required for the elicitation of delayed-type hypersensitivity (DTH) in mice. In the current study, light microscopic radioautographs from animals treated with [3H]5-HT indicated that local mast cells released 5-HT between 6 and 18 h during the evolution of DTH. Ultrastructural examination of mast cells revealed surface activation, indicated by extension of surface filopodia, and degranulation by fusion and exocytosis. Light and electron microscopic studies of the endothelium of postcapillary venules at sites of DTH revealed the development of gaps between adjacent cells. The development of gaps permitted extravasation of tracers that was abolished by depletion or antagonism of 5-HT. Thus mast cells degranulated and released 5-HT in DTH, and this 5-HT acted on local vessels. Recipients of nonadherent, non-immunoglobulin-bearing sensitized lymphocytes also demonstrated similar mast cell degranulation and the formation of endothelial gaps. This indicated that mast cell degranulation and 5-HT release in murine DTH were probably T cell dependent.