IgA Nephropathy: Molecular Mechanisms of the Disease

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F13%3A10190352" target="_blank" >RIV/00216208:11110/13:10190352 - isvavai.cz</a>

Alternative codes found

RIV/61388971:_____/13:00426184 RIV/61989592:15110/13:33140778 RIV/00216208:11130/13:10190352 RIV/00064203:_____/13:10190352

Result on the web

<a href="http://dx.doi.org/10.1146/annurev-pathol-011110-130216" target="_blank" >http://dx.doi.org/10.1146/annurev-pathol-011110-130216</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1146/annurev-pathol-011110-130216" target="_blank" >10.1146/annurev-pathol-011110-130216</a>

Result language

angličtina

Original language name

IgA Nephropathy: Molecular Mechanisms of the Disease

Original language description

Studies of molecular and cellular interactions involved in the pathogenesis of IgA nephropathy have revealed the autoimmune nature of this most common primary glomerulonephritis. In patients with this disease, altered glycan structures in the unique hinge region of the heavy chains of IgA1 molecules lead to the exposure of antigenic determinants, which are recognized by naturally occurring antiglycan antibodies of the IgG and/or IgA1 isotype. As a result, nephritogenic immune complexes form in the circulation and deposit in the glomerular mesangium. Deposited immune complexes induce proliferation of resident mesangial cells, increased production of extracellular matrix proteins and cytokines, and ultimately loss of glomerular function. Structural elucidation of the nature of these immune complexes and their biological activity should provide a rational basis for an effective, immunologically mediated inhibition of the formation of nephritogenic immune complexes that could be used as a

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

EC - Immunology

OECD FORD branch

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Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Publication year

2013

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Annual Review of Pathology: Mechanisms of Disease

ISSN

1553-4006

e-ISSN

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Volume of the periodical

8

Issue of the periodical within the volume

Jan 24

Country of publishing house

US - UNITED STATES

Number of pages

24

Pages from-to

217-240

UT code for WoS article

000318483400009

EID of the result in the Scopus database

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