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Statements

Subject Item
n2:RIV%2F61989592%3A15110%2F13%3A33140778%21RIV14-MZ0-15110___
rdf:type
n14:Vysledek skos:Concept
dcterms: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 disease-specific therapeutic approach. 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 disease-specific therapeutic approach.
dcterms:title
IgA Nephropathy: Molecular Mechanisms of the Disease IgA Nephropathy: Molecular Mechanisms of the Disease
skos:prefLabel
IgA Nephropathy: Molecular Mechanisms of the Disease IgA Nephropathy: Molecular Mechanisms of the Disease
skos:notation
RIV/61989592:15110/13:33140778!RIV14-MZ0-15110___
n14:predkladatel
n15:orjk%3A15110
n4:aktivita
n16:V n16:P n16:I
n4:aktivity
I, P(GAP302/10/1055), P(LH11046), P(NT11081), V
n4:cisloPeriodika
8
n4:dodaniDat
n5:2014
n4:domaciTvurceVysledku
n13:1587307
n4:druhVysledku
n18:J
n4:duvernostUdaju
n17:S
n4:entitaPredkladatele
n11:predkladatel
n4:idSjednocenehoVysledku
78803
n4:idVysledku
RIV/61989592:15110/13:33140778
n4:jazykVysledku
n10:eng
n4:klicovaSlova
IgA nephropathy
n4:klicoveSlovo
n7:IgA%20nephropathy
n4:kodStatuVydavatele
US - Spojené státy americké
n4:kontrolniKodProRIV
[94DA105E1BAD]
n4:nazevZdroje
Annual Review of Pathology-Mechanisms of Disease
n4:obor
n12:EC
n4:pocetDomacichTvurcuVysledku
1
n4:pocetTvurcuVysledku
9
n4:projekt
n6:LH11046 n6:GAP302%2F10%2F1055 n6:NT11081
n4:rokUplatneniVysledku
n5:2013
n4:svazekPeriodika
2013
n4:tvurceVysledku
Novák, Lea Julian, Bruce Gharavi, Ali Renfrow, Matthew Matoušovic, Karel Městecký, Jiří Moldoveanu, Zina Raška, Milan Novák, Jan
n4:wos
000318483400009
s:issn
1553-4006
s:numberOfPages
24
n20:doi
10.1146/annurev-pathol-011110-130216
n19:organizacniJednotka
15110