A. Hassan, Ihab Z. El-Hakim, N. Amr, D. El-Ghoneimy, D. Soliman, D. Sallam
{"title":"干扰素γ:它是特发性肾病综合征发病机制的共同参与者吗?","authors":"A. Hassan, Ihab Z. El-Hakim, N. Amr, D. El-Ghoneimy, D. Soliman, D. Sallam","doi":"10.21608/ejpa.2020.81768","DOIUrl":null,"url":null,"abstract":"Introduction: Idiopathic nephrotic syndrome (INS), the most common form of NS in childhood, was considered 4 decades ago as a systemic disorder of T cells, mediated through its released cytokines. To date, the exact incriminated cytokine or immunological mediator is not properly defined. Interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, is thought to have a role in the provocation of the T cell-mediated INS relapse, through the promotion of T helper1 (Th1) differentiation and suppression of regulatory T cells (Treg). Aim of the study: To evaluate the immunopathogenic role of IFN-gamma in children with steroid-sensitive idiopathic nephrotic syndrome (SSNS) through monitoring the changes in its levels with disease course. Methods: This study included twenty-five newly diagnosed children with SSINS. They were all given full dose prednisolone, evaluated at initial diagnosis and at full remission as regards the serum level of IFN-gamma. Results: Serum levels of IFN-gamma were lowermost at the time of diagnosis and increased with remission on corticosteroids. Conclusions: This study points to a role for the lower serum IFN-gamma at diagnosis, in the immunopathogenesis of INS than at remission and the rise in its serum level might be a marker of remission induction, however, this awaits confirmation in larger-scale studies. Studies on renal biopsy specimens are needed to determine the exact renal in situ levels and effects of IFN-gamma","PeriodicalId":52068,"journal":{"name":"Egyptian Journal of Pediatric Allergy and Immunology","volume":null,"pages":null},"PeriodicalIF":0.2000,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Interferon gamma: is it a co-player in the pathogenesis of idiopathic nephrotic syndrome?\",\"authors\":\"A. Hassan, Ihab Z. El-Hakim, N. Amr, D. El-Ghoneimy, D. Soliman, D. Sallam\",\"doi\":\"10.21608/ejpa.2020.81768\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction: Idiopathic nephrotic syndrome (INS), the most common form of NS in childhood, was considered 4 decades ago as a systemic disorder of T cells, mediated through its released cytokines. To date, the exact incriminated cytokine or immunological mediator is not properly defined. Interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, is thought to have a role in the provocation of the T cell-mediated INS relapse, through the promotion of T helper1 (Th1) differentiation and suppression of regulatory T cells (Treg). Aim of the study: To evaluate the immunopathogenic role of IFN-gamma in children with steroid-sensitive idiopathic nephrotic syndrome (SSNS) through monitoring the changes in its levels with disease course. Methods: This study included twenty-five newly diagnosed children with SSINS. They were all given full dose prednisolone, evaluated at initial diagnosis and at full remission as regards the serum level of IFN-gamma. Results: Serum levels of IFN-gamma were lowermost at the time of diagnosis and increased with remission on corticosteroids. Conclusions: This study points to a role for the lower serum IFN-gamma at diagnosis, in the immunopathogenesis of INS than at remission and the rise in its serum level might be a marker of remission induction, however, this awaits confirmation in larger-scale studies. Studies on renal biopsy specimens are needed to determine the exact renal in situ levels and effects of IFN-gamma\",\"PeriodicalId\":52068,\"journal\":{\"name\":\"Egyptian Journal of Pediatric Allergy and Immunology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.2000,\"publicationDate\":\"2020-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Egyptian Journal of Pediatric Allergy and Immunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.21608/ejpa.2020.81768\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"ALLERGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Egyptian Journal of Pediatric Allergy and Immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21608/ejpa.2020.81768","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ALLERGY","Score":null,"Total":0}
Interferon gamma: is it a co-player in the pathogenesis of idiopathic nephrotic syndrome?
Introduction: Idiopathic nephrotic syndrome (INS), the most common form of NS in childhood, was considered 4 decades ago as a systemic disorder of T cells, mediated through its released cytokines. To date, the exact incriminated cytokine or immunological mediator is not properly defined. Interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, is thought to have a role in the provocation of the T cell-mediated INS relapse, through the promotion of T helper1 (Th1) differentiation and suppression of regulatory T cells (Treg). Aim of the study: To evaluate the immunopathogenic role of IFN-gamma in children with steroid-sensitive idiopathic nephrotic syndrome (SSNS) through monitoring the changes in its levels with disease course. Methods: This study included twenty-five newly diagnosed children with SSINS. They were all given full dose prednisolone, evaluated at initial diagnosis and at full remission as regards the serum level of IFN-gamma. Results: Serum levels of IFN-gamma were lowermost at the time of diagnosis and increased with remission on corticosteroids. Conclusions: This study points to a role for the lower serum IFN-gamma at diagnosis, in the immunopathogenesis of INS than at remission and the rise in its serum level might be a marker of remission induction, however, this awaits confirmation in larger-scale studies. Studies on renal biopsy specimens are needed to determine the exact renal in situ levels and effects of IFN-gamma