{"title":"糖皮质激素在体外诱导Th2反应。","authors":"F Ramírez","doi":"10.1155/1998/73401","DOIUrl":null,"url":null,"abstract":"<p><p>Purified rat CD4+ T cells were activated in vitro, by the polyclonal mitogen Concanavalin A (Con A) or by mixed lymphocyte reaction (MLR), in the presence or absence of the glucocorticoid dexamethasone (DEX). They were then expanded in IL-2 and subsequently restimulated, this time in the absence of the hormone. The results indicate that the exposure of the cells to DEX in the primary stimulation changed the cytokine synthesis induced by the secondary stimulation. IL-4 production was increased by the pretreatment whereas synthesis of IFN-gamma was diminished. Addition of DEX in the second activation suppressed all cytokine production. In brief, the transient presence of glucocorticoids in the culture induces a change in the pattern of cytokine production but the continuous presence causes inhibition of cytokine synthesis. Further studies in which IL-4 was used together with DEX showed that the cytokine potentiated the effect of the hormone. The data here presented suggest that glucocorticoids and the neuroendocrine system may be expected to have long-term immunological effects as well as short-lived immunosuppressive ones. High concentration of glucocorticoids suppress cytokine production but when steroids return to basal levels the immune response is directed in a way that favors Th2-type reactions. Possible implications regarding the immune response to pathogens and autoantigens are discussed.</p>","PeriodicalId":77106,"journal":{"name":"Developmental immunology","volume":"6 3-4","pages":"233-43"},"PeriodicalIF":0.0000,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/1998/73401","citationCount":"56","resultStr":"{\"title\":\"Glucocorticoids induce a Th2 response in vitro.\",\"authors\":\"F Ramírez\",\"doi\":\"10.1155/1998/73401\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Purified rat CD4+ T cells were activated in vitro, by the polyclonal mitogen Concanavalin A (Con A) or by mixed lymphocyte reaction (MLR), in the presence or absence of the glucocorticoid dexamethasone (DEX). They were then expanded in IL-2 and subsequently restimulated, this time in the absence of the hormone. The results indicate that the exposure of the cells to DEX in the primary stimulation changed the cytokine synthesis induced by the secondary stimulation. IL-4 production was increased by the pretreatment whereas synthesis of IFN-gamma was diminished. Addition of DEX in the second activation suppressed all cytokine production. In brief, the transient presence of glucocorticoids in the culture induces a change in the pattern of cytokine production but the continuous presence causes inhibition of cytokine synthesis. Further studies in which IL-4 was used together with DEX showed that the cytokine potentiated the effect of the hormone. The data here presented suggest that glucocorticoids and the neuroendocrine system may be expected to have long-term immunological effects as well as short-lived immunosuppressive ones. High concentration of glucocorticoids suppress cytokine production but when steroids return to basal levels the immune response is directed in a way that favors Th2-type reactions. Possible implications regarding the immune response to pathogens and autoantigens are discussed.</p>\",\"PeriodicalId\":77106,\"journal\":{\"name\":\"Developmental immunology\",\"volume\":\"6 3-4\",\"pages\":\"233-43\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1998-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1155/1998/73401\",\"citationCount\":\"56\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Developmental immunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1155/1998/73401\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Developmental immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/1998/73401","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 56
摘要
在糖皮质激素地塞米松(DEX)存在或不存在的情况下,纯化的大鼠CD4+ T细胞在体外被多克隆丝裂原Concanavalin A (Con A)或混合淋巴细胞反应(MLR)激活。然后它们在IL-2中扩大,随后在缺乏激素的情况下重新受到刺激。结果表明,在一次刺激下,细胞暴露于DEX改变了二次刺激诱导的细胞因子合成。预处理增加了IL-4的产生,而减少了ifn - γ的合成。在第二次激活中加入DEX抑制了所有细胞因子的产生。简而言之,培养物中糖皮质激素的短暂存在会引起细胞因子产生模式的变化,但持续存在会导致细胞因子合成的抑制。进一步的研究表明,IL-4与DEX一起使用,细胞因子增强了激素的作用。这里提出的数据表明,糖皮质激素和神经内分泌系统可能具有长期的免疫作用以及短期的免疫抑制作用。高浓度的糖皮质激素会抑制细胞因子的产生,但当类固醇恢复到基础水平时,免疫反应会朝着有利于th2型反应的方向发展。对病原体和自身抗原的免疫反应可能的影响进行了讨论。
Purified rat CD4+ T cells were activated in vitro, by the polyclonal mitogen Concanavalin A (Con A) or by mixed lymphocyte reaction (MLR), in the presence or absence of the glucocorticoid dexamethasone (DEX). They were then expanded in IL-2 and subsequently restimulated, this time in the absence of the hormone. The results indicate that the exposure of the cells to DEX in the primary stimulation changed the cytokine synthesis induced by the secondary stimulation. IL-4 production was increased by the pretreatment whereas synthesis of IFN-gamma was diminished. Addition of DEX in the second activation suppressed all cytokine production. In brief, the transient presence of glucocorticoids in the culture induces a change in the pattern of cytokine production but the continuous presence causes inhibition of cytokine synthesis. Further studies in which IL-4 was used together with DEX showed that the cytokine potentiated the effect of the hormone. The data here presented suggest that glucocorticoids and the neuroendocrine system may be expected to have long-term immunological effects as well as short-lived immunosuppressive ones. High concentration of glucocorticoids suppress cytokine production but when steroids return to basal levels the immune response is directed in a way that favors Th2-type reactions. Possible implications regarding the immune response to pathogens and autoantigens are discussed.