Fariha Kanwal, A. Simair, Ting Chen, Yunlon Zhang, I. Qadri, Changrui Lu
{"title":"Molecular Cloning and In Silico Analysis of hIL-6 Gene from Pakistani Dengue Hemorrhagic Fever Patients","authors":"Fariha Kanwal, A. Simair, Ting Chen, Yunlon Zhang, I. Qadri, Changrui Lu","doi":"10.15406/moji.2017.05.00170","DOIUrl":null,"url":null,"abstract":"Interleukin 6 (IL-6) is an important player against infections and tissue damage in mammalian host defense. Its biological functions are evidently spacious including hematopoiesis, modulation of immune response, regulation of endocrine and nervous systems, protective plasma proteins, acute-phase proteins by the liver and control of body temperature [1-3]. IL-6 works in an expansive manner on cells of the immune and nonimmune system and most often behave like a hormone affecting homeostatic processes. Its prompt induction starts with the onset of any tissue damage or inflammation, activating the host defense and terminates upon tissue homeostasis restoration [4,5]. However, the deregulated persistent synthesis of IL-6 has been seen in the development of various autoimmune, chronic inflammatory diseases and cancers [6]. Clinical trials using the humanized anti-IL-6 receptor monoclonal antibody have verified the efficacy of IL-6 blockade for the treatment of unmanageable inflammatory diseases, such as systemic juvenile idiopathic arthritis, rheumatoid arthritis, and Castleman’s disease. Its situation-dependent pro and anti-inflammatory nature makes cytokine as a top intention for clinical intervention [7-10]. However, IL-6 have several alternative molecular forms with multi-pattern post-translational modifications but its diverse cellular response is unclear and the recombinant IL-6 from bacteria without modifications reproducing all known functions left these post-translational modifications as non-causative for diverse actions of IL-6 [11,12].","PeriodicalId":90928,"journal":{"name":"MOJ immunology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"MOJ immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15406/moji.2017.05.00170","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Interleukin 6 (IL-6) is an important player against infections and tissue damage in mammalian host defense. Its biological functions are evidently spacious including hematopoiesis, modulation of immune response, regulation of endocrine and nervous systems, protective plasma proteins, acute-phase proteins by the liver and control of body temperature [1-3]. IL-6 works in an expansive manner on cells of the immune and nonimmune system and most often behave like a hormone affecting homeostatic processes. Its prompt induction starts with the onset of any tissue damage or inflammation, activating the host defense and terminates upon tissue homeostasis restoration [4,5]. However, the deregulated persistent synthesis of IL-6 has been seen in the development of various autoimmune, chronic inflammatory diseases and cancers [6]. Clinical trials using the humanized anti-IL-6 receptor monoclonal antibody have verified the efficacy of IL-6 blockade for the treatment of unmanageable inflammatory diseases, such as systemic juvenile idiopathic arthritis, rheumatoid arthritis, and Castleman’s disease. Its situation-dependent pro and anti-inflammatory nature makes cytokine as a top intention for clinical intervention [7-10]. However, IL-6 have several alternative molecular forms with multi-pattern post-translational modifications but its diverse cellular response is unclear and the recombinant IL-6 from bacteria without modifications reproducing all known functions left these post-translational modifications as non-causative for diverse actions of IL-6 [11,12].