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The role of IgA in the pathogenesis of IgA nephropathy
ID Perše, Martina (Author), ID Večerić-Haler, Željka (Author)

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Abstract
Immunoglobulin A (IgA) is the most abundant antibody isotype produced in humans, predominantly present in the mucosal areas where its main functions are the neutralization of toxins, prevention of microbial invasion across the mucosal epithelial barrier, and simultaneous maintenance of a physiologically indispensable symbiotic relationship with commensal bacteria. The process of IgA biosynthesis, interaction with receptors, and clearance can be disrupted in certain pathologies, like IgA nephropathy, which is the most common form of glomerulonephritis worldwide. This review summarizes the latest findings in the complex characteristics of the molecular structure and biological functions of IgA antibodies, offering an in-depth overview of recent advances in the understanding of biochemical, immunologic, and genetic factors important in the pathogenesis of IgA nephropathy.

Language:English
Keywords:IgA, IgA nephropathy, mucosal immunity, immunoglobulin A
Work type:Article
Typology:1.02 - Review Article
Organization:MF - Faculty of Medicine
Publication status:Published
Publication version:Version of Record
Year:2019
Number of pages:19 str.
Numbering:Vol. 20, iss. 24, art. 6199
PID:20.500.12556/RUL-133107 This link opens in a new window
UDC:616.6
ISSN on article:1422-0067
DOI:10.3390/ijms20246199 This link opens in a new window
COBISS.SI-ID:6761388 This link opens in a new window
Publication date in RUL:11.11.2021
Views:468
Downloads:122
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Record is a part of a journal

Title:International journal of molecular sciences
Shortened title:Int. j. mol. sci.
Publisher:MDPI
ISSN:1422-0067
COBISS.SI-ID:2779162 This link opens in a new window

Licences

License:CC BY 4.0, Creative Commons Attribution 4.0 International
Link:http://creativecommons.org/licenses/by/4.0/
Description:This is the standard Creative Commons license that gives others maximum freedom to do what they want with the work as long as they credit the author.
Licensing start date:09.12.2019

Projects

Funder:ARRS - Slovenian Research Agency
Project number:P3-0054
Name:Patologija in molekularna genetika

Funder:ARRS - Slovenian Research Agency
Project number:P3-0323
Name:Ledvične bolezni in nadomestna zdravljenja

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