Cellular Signaling and Production of Galactose-Deficient IgA1 in IgA Nephropathy, an Autoimmune Disease
المؤلفون المشاركون
Julian, Bruce A.
Reily, Colin
Ueda, Hiroyuki
Huang, Zhi-Qiang
Willey, Christopher D.
Novak, Jan
Mestecky, Jiri
المصدر
Journal of Immunology Research
العدد
المجلد 2014، العدد 2014 (31 ديسمبر/كانون الأول 2014)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2014-07-23
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص EN
Immunoglobulin A (IgA) nephropathy (IgAN), the leading cause of primary glomerulonephritis, is characterized by IgA1-containing immunodeposits in the glomeruli.
IgAN is a chronic disease, with up to 40% of patients progressing to end-stage renal disease, with no disease-specific treatment.
Multiple studies of the origin of the glomerular immunodeposits have linked elevated circulating levels of aberrantly glycosylated IgA1 (galactose-deficient in some O-glycans; Gd-IgA1) with formation of nephritogenic Gd-IgA1-containing immune complexes.
Gd-IgA1 is recognized as an autoantigen in susceptible individuals by anti-glycan autoantibodies, resulting in immune complexes that may ultimately deposit in the kidney and induce glomerular injury.
Genetic studies have revealed that an elevated level of Gd-IgA1 in the circulation of IgAN patients is a hereditable trait.
Moreover, recent genome-wide association studies have identified several immunity-related loci that associated with IgAN.
Production of Gd-IgA1 by IgA1-secreting cells of IgAN patients has been attributed to abnormal expression and activity of several key glycosyltransferases.
Substantial evidence is emerging that abnormal signaling in IgA1-producing cells is related to the production of Gd-IgA1.
As Gd-IgA1 is the key autoantigen in IgAN, understanding the genetic, biochemical, and environmental aspects of the abnormal signaling in IgA1-producing cells will provide insight into possible targets for future disease-specific therapy.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Reily, Colin& Ueda, Hiroyuki& Huang, Zhi-Qiang& Mestecky, Jiri& Julian, Bruce A.& Willey, Christopher D.…[et al.]. 2014. Cellular Signaling and Production of Galactose-Deficient IgA1 in IgA Nephropathy, an Autoimmune Disease. Journal of Immunology Research،Vol. 2014, no. 2014, pp.1-10.
https://search.emarefa.net/detail/BIM-1040789
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Reily, Colin…[et al.]. Cellular Signaling and Production of Galactose-Deficient IgA1 in IgA Nephropathy, an Autoimmune Disease. Journal of Immunology Research No. 2014 (2014), pp.1-10.
https://search.emarefa.net/detail/BIM-1040789
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Reily, Colin& Ueda, Hiroyuki& Huang, Zhi-Qiang& Mestecky, Jiri& Julian, Bruce A.& Willey, Christopher D.…[et al.]. Cellular Signaling and Production of Galactose-Deficient IgA1 in IgA Nephropathy, an Autoimmune Disease. Journal of Immunology Research. 2014. Vol. 2014, no. 2014, pp.1-10.
https://search.emarefa.net/detail/BIM-1040789
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1040789
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر