Alterations in Early Biochemical Events Following T Cell Activation in Leprosy Patients

Nidhi Sharma , V.K. Sharma , Anu Gupta , Inderjeet Kaur , Sukhbir Kaur , N.K. Ganguly
{"title":"Alterations in Early Biochemical Events Following T Cell Activation in Leprosy Patients","authors":"Nidhi Sharma ,&nbsp;V.K. Sharma ,&nbsp;Anu Gupta ,&nbsp;Inderjeet Kaur ,&nbsp;Sukhbir Kaur ,&nbsp;N.K. Ganguly","doi":"10.1006/clin.1998.4543","DOIUrl":null,"url":null,"abstract":"<div><p>The early events of activation and cytokine profiles (IL-2, 4, and 6) were studied in lymphocytes of paucibacillary (TT/BT) and multibacillary (BL/LL) leprosy patients after stimulation with PMA/A23187 and<em>Mycobacterium leprae</em>antigen (PGL-1). Lymphocytes from BT/TT patients showed proliferation in response to both PMA/A23187 and PGL-1 compared to BL/LL. The levels of early activation signaling molecules such as IP<sub>3</sub>, calcium, and protein kinase C (PKC) in the particulate fraction were found to be elevated in BT/TT and BL/LL patients and showed a further significant increase after stimulation with PMA/A23187 in BT/TT patients. PGL-1 marginally increased the IP<sub>3</sub>levels in BT/TT patients, whereas in BL/LL patients, it had no effect. The levels of IL-2 were enhanced in lymphocytes of BT/TT leprosy patients and were further augmented by PPD and PGL-1, while the levels of IL-4 and IL-6 were increased in LL/BL lymphocytes and further augmented by PGL-1. Thus PGL-1 seems to be a major culprit in inducing the T<sub>H</sub>2-type cytokine response observed in lepromatous leprosy patients.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"88 2","pages":"Pages 142-149"},"PeriodicalIF":0.0000,"publicationDate":"1998-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4543","citationCount":"10","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical immunology and immunopathology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0090122998945433","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 10

Abstract

The early events of activation and cytokine profiles (IL-2, 4, and 6) were studied in lymphocytes of paucibacillary (TT/BT) and multibacillary (BL/LL) leprosy patients after stimulation with PMA/A23187 andMycobacterium lepraeantigen (PGL-1). Lymphocytes from BT/TT patients showed proliferation in response to both PMA/A23187 and PGL-1 compared to BL/LL. The levels of early activation signaling molecules such as IP3, calcium, and protein kinase C (PKC) in the particulate fraction were found to be elevated in BT/TT and BL/LL patients and showed a further significant increase after stimulation with PMA/A23187 in BT/TT patients. PGL-1 marginally increased the IP3levels in BT/TT patients, whereas in BL/LL patients, it had no effect. The levels of IL-2 were enhanced in lymphocytes of BT/TT leprosy patients and were further augmented by PPD and PGL-1, while the levels of IL-4 and IL-6 were increased in LL/BL lymphocytes and further augmented by PGL-1. Thus PGL-1 seems to be a major culprit in inducing the TH2-type cytokine response observed in lepromatous leprosy patients.

麻风病患者T细胞活化后早期生化事件的改变
研究了PMA/A23187和麻风分枝杆菌抗原(PGL-1)刺激少杆菌(TT/BT)和多杆菌(BL/LL)麻风患者淋巴细胞的早期活化事件和细胞因子(IL-2、4和6)谱。与BL/LL相比,BT/TT患者淋巴细胞对PMA/A23187和PGL-1均有增殖反应。BT/TT和BL/LL患者颗粒组分中IP3、钙、PKC等早期激活信号分子水平升高,BT/TT患者PMA/A23187刺激后IP3、钙、PKC水平进一步显著升高。PGL-1在BT/TT患者中略微增加ip3水平,而在BL/LL患者中没有作用。BT/TT麻风患者淋巴细胞中IL-2水平升高,PPD和PGL-1使其进一步升高;LL/BL淋巴细胞中IL-4和IL-6水平升高,PGL-1使其进一步升高。因此,PGL-1似乎是诱导麻风患者中观察到的th2型细胞因子反应的主要罪魁祸首。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信