{"title":"白细胞介素(IL)-12和干扰素-γ诱导因子/IL-18在小鼠实验性麻风分枝杆菌感染中的可能作用","authors":"Kazuo Kobayashi , Masanori Kai , Masa-ichi Gidoh , Noboru Nakata , Masumi Endoh , Ram Pyare Singh , Tsuyoshi Kasama , Hajime Saito","doi":"10.1006/clin.1998.4533","DOIUrl":null,"url":null,"abstract":"<div><p>Cell-mediated immunity participates in host defense against mycobacterial infection. Both interleukin 12 (IL-12) and interferon-γ-inducing factor (IGIF/IL-18), produced mainly by macrophages, play a critical role in expression of cell-mediated immunity. To investigate the role of IL-12 and IGIF/IL-18<em>in vivo,</em>we examined cytokine profile, bacterial growth, and the potential benefit of cytokine therapy in susceptible and resistant mice infected with<em>Mycobacterium leprae.</em>The early expression of IL-12 p40 and IGIF/IL-18 at the site of inoculation was found in resistant mice 3–72 h after the infection, but not in susceptible mice. Both strains of mice did not show expression of IFN-γ and IL-4. IL-12 administration resulted in a significant reduction of bacterial counts in mice with established<em>M. leprae</em>infection. The results imply that susceptible mice exhibit decreased expression of type 1 helper T (Th1) response without reciprocal increased Th2 response and show responsiveness to exogenous IL-12. IL-12 therapy may be a possible rationale for treatment of<em>M. leprae</em>infection.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"88 3","pages":"Pages 226-231"},"PeriodicalIF":0.0000,"publicationDate":"1998-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4533","citationCount":"80","resultStr":"{\"title\":\"The Possible Role of Interleukin (IL)-12 and Interferon-γ-Inducing Factor/IL-18 in Protection against ExperimentalMycobacterium lepraeInfection in Mice\",\"authors\":\"Kazuo Kobayashi , Masanori Kai , Masa-ichi Gidoh , Noboru Nakata , Masumi Endoh , Ram Pyare Singh , Tsuyoshi Kasama , Hajime Saito\",\"doi\":\"10.1006/clin.1998.4533\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Cell-mediated immunity participates in host defense against mycobacterial infection. Both interleukin 12 (IL-12) and interferon-γ-inducing factor (IGIF/IL-18), produced mainly by macrophages, play a critical role in expression of cell-mediated immunity. To investigate the role of IL-12 and IGIF/IL-18<em>in vivo,</em>we examined cytokine profile, bacterial growth, and the potential benefit of cytokine therapy in susceptible and resistant mice infected with<em>Mycobacterium leprae.</em>The early expression of IL-12 p40 and IGIF/IL-18 at the site of inoculation was found in resistant mice 3–72 h after the infection, but not in susceptible mice. Both strains of mice did not show expression of IFN-γ and IL-4. IL-12 administration resulted in a significant reduction of bacterial counts in mice with established<em>M. leprae</em>infection. The results imply that susceptible mice exhibit decreased expression of type 1 helper T (Th1) response without reciprocal increased Th2 response and show responsiveness to exogenous IL-12. IL-12 therapy may be a possible rationale for treatment of<em>M. leprae</em>infection.</p></div>\",\"PeriodicalId\":10683,\"journal\":{\"name\":\"Clinical immunology and immunopathology\",\"volume\":\"88 3\",\"pages\":\"Pages 226-231\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1998-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1006/clin.1998.4533\",\"citationCount\":\"80\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical immunology and immunopathology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0090122998945330\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical immunology and immunopathology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0090122998945330","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 80
摘要
细胞介导的免疫参与宿主对分枝杆菌感染的防御。白细胞介素12 (IL-12)和干扰素γ诱导因子(IGIF/IL-18)主要由巨噬细胞产生,在细胞介导免疫的表达中起关键作用。为了研究IL-12和IGIF/ il -18在体内的作用,我们检测了感染麻风分枝杆菌的易感和耐药小鼠的细胞因子谱、细菌生长以及细胞因子治疗的潜在益处。感染后3 ~ 72 h,耐药小鼠接种部位IL-12 p40和IGIF/IL-18均有早期表达,而易感小鼠无。两株小鼠均未显示IFN-γ和IL-4的表达。IL-12给药可显著减少小鼠的细菌计数。lepraeinfection。结果表明,易感小鼠表现出1型辅助性T (Th1)反应的表达降低,而Th2反应没有相应的增加,并对外源性IL-12表现出应答性。IL-12治疗可能是治疗多发性硬化症的基本原理。lepraeinfection。
The Possible Role of Interleukin (IL)-12 and Interferon-γ-Inducing Factor/IL-18 in Protection against ExperimentalMycobacterium lepraeInfection in Mice
Cell-mediated immunity participates in host defense against mycobacterial infection. Both interleukin 12 (IL-12) and interferon-γ-inducing factor (IGIF/IL-18), produced mainly by macrophages, play a critical role in expression of cell-mediated immunity. To investigate the role of IL-12 and IGIF/IL-18in vivo,we examined cytokine profile, bacterial growth, and the potential benefit of cytokine therapy in susceptible and resistant mice infected withMycobacterium leprae.The early expression of IL-12 p40 and IGIF/IL-18 at the site of inoculation was found in resistant mice 3–72 h after the infection, but not in susceptible mice. Both strains of mice did not show expression of IFN-γ and IL-4. IL-12 administration resulted in a significant reduction of bacterial counts in mice with establishedM. lepraeinfection. The results imply that susceptible mice exhibit decreased expression of type 1 helper T (Th1) response without reciprocal increased Th2 response and show responsiveness to exogenous IL-12. IL-12 therapy may be a possible rationale for treatment ofM. lepraeinfection.