Requirement for vasoactive amines for production of delayed-type hypersensitvity skin reactions.
Requirement for vasoactive amines for production of delayed-type hypersensitvity skin reactions.
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产生迟发型过敏性皮肤反应需要血管活性胺。
DOI：
10.1084/jem.142.3.732
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发表时间：
1975-09-01
影响因子：
15.3
通讯作者：
Gershon, M D
中科院分区：
文献类型：
--
作者：
Gershon, R K;Askenase, P W;Gershon, M D
小鼠最容易引发迟发型超敏反应 (DTH) 反应的皮肤部位（足垫和耳朵）特别富含含有 5-羟色胺 (5-HT) 的肥大细胞。由于小鼠缺乏循环嗜碱性粒细胞，而嗜碱性粒细胞至少在某些 DTH 反应中发挥作用，因此我们研究了肥大细胞在小鼠 DTH 皮肤反应的演变中发挥重要作用的可能性。我们发现利血平（一种消耗 5-HT 肥大细胞的药物）消除了小鼠皮肤中 DTH 反应的能力。利血平的抑制作用可以被单胺氧化酶抑制剂部分阻断，单胺氧化酶抑制剂可防止肥大细胞胞浆中 5-HT 的降解。经利血平治疗的免疫小鼠的脾细胞正常地将 DTH 反应转移至非免疫小鼠，表明利血平治疗不会影响免疫 T 细胞。 DTH 反应不能转移到利血平治疗的小鼠中。我们认为，T 细胞通过毛细血管后微静脉内皮，通过不依赖于血管活性胺的机制，不断从血液中迁移出来。如果它们具有适当的免疫能力并遇到组织中的同源抗原，它们会诱导肥大细胞释放血管活性胺，导致毛细血管后微静脉内皮细胞分离，从而使通常不再循环的细胞从血液中排出。随后到达的血管活性胺依赖性细胞负责 DTH 反应的微观和宏观损伤。趋化因子也可能参与将细胞带到 DTH 反应位点，但我们提出 T 细胞对血管活性含胺细胞的调节允许效应细胞在被调用后通过内皮门。
The skin sites of the mouse where delayed-type hypersensitivity (DTH) reactions are most easily elicited (foot pads and ears) are particularly rich in 5-hydroxytryptamine (5-HT)-containing mast cells. Since mice are deficient in circulating basophils, which play a role in at least some DTH reactions, we investigated the possibility that the mast cells were playing an important role in the evolution of the skin reactions of DTH in mice. We found that reserpine, a drug which depletes mast cells of 5-HT, abolished the ability of the mouse to make DTH reactions in the skin. The suppressive effect of reserpine could be partially blocked by monoamine oxidase inhibitors which prevent the degradation of 5-HT in the cytosol of the mast cell. Spleen cells of immune, reserpine-treated mice transferred DTH reactions to nonimmune mice normally, indicating that the reserpine treatment did not affect immune T cells. DTH reactions could not be transferred into reserpine- treated mice. We suggest that T cells are continually emigrating from the blood, through postcapillary venule endothelium, by a mechanism which does not depend on vasoactive amines. If they are appropriately immune and meet the homologous antigen in the tissue, they induce mast cells to release vasoactive amines which cause postcapillary venule endothelial cells to separate, allowing the egress from the blood of cells which ordinarily do not recirculate. The secondarily arriving vasoactive amine-dependent cells are responsible for the micro- and macroscopic lesions of DTH reactions. Chemotactic factors may also be involved in bringing cells to the DTH reaction sites but we propose that T-cell regulation of vasoactive amine-containing cells allows the effector cells to pass through the endothelial gates after they are called.