ADVANCEMENT IN THERAPEUTIC EFFORTS AND TOOLS FOR PREVENTION AND TREATMENT OF INSULIN DEPENDENT DIABETES MELLITIS

Imran Qadir
{"title":"ADVANCEMENT IN THERAPEUTIC EFFORTS AND TOOLS FOR PREVENTION AND TREATMENT OF INSULIN DEPENDENT DIABETES MELLITIS","authors":"Imran Qadir","doi":"10.22200/PJPR.20172%P","DOIUrl":null,"url":null,"abstract":"Insulin Dependent Diabetes Mellitus (IDDM) is an autoimmune disease and is also called type 1diabetes. It occurs mostly due to CD8+ and CD4+ T lymphocytes which are actually the T-helper cells and very rarely by some virus and drugs which take the β-cells, insulin and proinsulin as its target. Th-cells may also affect by other ways i.e. by secreting the CXCL10 which are also reactive against the β-cells. In these patients there is low level of insulin causing high level of glucose also called hyperglycemia. To treat this autoimmune disorder we take some important steps either against the autoimmune responses or in the favor of proliferation of the β-cells or may take steps for the production of the insulin by either ways. There is possibility to give the patients monoclonal antibodies against the causative agents. We can also use the stem cells from pancreas that can grow to the new matured functional islet of langerhan. Moreover replacement of beta cell mass, non-endocrine cell production, antigen-based therapy, pancreatic transplantation, use of immunosuppressive monocyte and control of IDDM by using naturally found CD4 + CD25 +, regulator of T lymphocytes, are other approaches. If we come to know the exact mechanism of CXCL10/CXCR3 system it may also be useful for us to treat the disease.","PeriodicalId":19952,"journal":{"name":"Pakistan Journal of Pharmaceutical Research","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2018-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pakistan Journal of Pharmaceutical Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22200/PJPR.20172%P","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

Abstract

Insulin Dependent Diabetes Mellitus (IDDM) is an autoimmune disease and is also called type 1diabetes. It occurs mostly due to CD8+ and CD4+ T lymphocytes which are actually the T-helper cells and very rarely by some virus and drugs which take the β-cells, insulin and proinsulin as its target. Th-cells may also affect by other ways i.e. by secreting the CXCL10 which are also reactive against the β-cells. In these patients there is low level of insulin causing high level of glucose also called hyperglycemia. To treat this autoimmune disorder we take some important steps either against the autoimmune responses or in the favor of proliferation of the β-cells or may take steps for the production of the insulin by either ways. There is possibility to give the patients monoclonal antibodies against the causative agents. We can also use the stem cells from pancreas that can grow to the new matured functional islet of langerhan. Moreover replacement of beta cell mass, non-endocrine cell production, antigen-based therapy, pancreatic transplantation, use of immunosuppressive monocyte and control of IDDM by using naturally found CD4 + CD25 +, regulator of T lymphocytes, are other approaches. If we come to know the exact mechanism of CXCL10/CXCR3 system it may also be useful for us to treat the disease.
胰岛素依赖型糖尿病的预防和治疗方法的研究进展
胰岛素依赖型糖尿病(IDDM)是一种自身免疫性疾病,也被称为1型糖尿病。它主要是由CD8+和CD4+ T淋巴细胞引起的它们实际上是T辅助细胞,很少由一些以β细胞,胰岛素和胰岛素原为靶点的病毒和药物引起。th细胞也可能通过其他方式产生影响,即分泌CXCL10, CXCL10也会对β细胞产生反应。在这些患者中,胰岛素水平低导致葡萄糖水平高,也称为高血糖症。为了治疗这种自身免疫性疾病,我们采取了一些重要的措施,要么对抗自身免疫反应,要么促进β细胞的增殖,要么通过这两种方式促进胰岛素的产生。有可能给予患者抗病原体的单克隆抗体。我们也可以利用胰腺的干细胞生长成新的成熟的功能胰岛。此外,替代β细胞群、非内分泌细胞生成、抗原治疗、胰腺移植、使用免疫抑制单核细胞和使用自然发现的CD4 + CD25 + (T淋巴细胞的调节剂)来控制IDDM也是其他方法。如果我们了解CXCL10/CXCR3系统的确切机制,也可能对我们治疗这种疾病有所帮助。
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
文献相关原料
公司名称 产品信息 采购帮参考价格
×
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