-
Something wrong with this record ?
IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease
J. Mestecky, BA. Julian, M. Raska
Language English Country Switzerland
Document type Journal Article, Review, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
NLK
Directory of Open Access Journals
from 2010
Free Medical Journals
from 2010
PubMed Central
from 2010
Europe PubMed Central
from 2010
Open Access Digital Library
from 2010-01-01
Open Access Digital Library
from 2010-01-01
ROAD: Directory of Open Access Scholarly Resources
from 2010
- MeSH
- Black People MeSH
- Child MeSH
- Glomerulonephritis, IGA * epidemiology ethnology MeSH
- Immunoglobulin A MeSH
- Antigen-Antibody Complex MeSH
- Epstein-Barr Virus Infections * epidemiology ethnology MeSH
- Infant MeSH
- Humans MeSH
- Adolescent MeSH
- Child, Preschool MeSH
- Herpesvirus 4, Human MeSH
- Check Tag
- Child MeSH
- Infant MeSH
- Humans MeSH
- Adolescent MeSH
- Child, Preschool MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Research Support, N.I.H., Extramural MeSH
- Geographicals
- Australia MeSH
IgA nephropathy (IgAN) is an autoimmune disease in which poorly galactosylated IgA1 is the antigen recognized by naturally occurring anti-glycan antibodies, leading to formation of nephritogenic circulating immune complexes. Incidence of IgAN displays geographical and racial disparity: common in Europe, North America, Australia, and east Asia, uncommon in African Americans, many Asian and South American countries, Australian Aborigines, and rare in central Africa. In analyses of sera and cells from White IgAN patients, healthy controls, and African Americans, IgAN patients exhibited substantial enrichment for IgA-expressing B cells infected with Epstein-Barr virus (EBV), leading to enhanced production of poorly galactosylated IgA1. Disparities in incidence of IgAN may reflect a previously disregarded difference in the maturation of the IgA system as related to the timing of EBV infection. Compared with populations with higher incidences of IgAN, African Americans, African Blacks, and Australian Aborigines are more frequently infected with EBV during the first 1-2 years of life at the time of naturally occurring IgA deficiency when IgA cells are less numerous than in late childhood or adolescence. Therefore, in very young children EBV enters "non-IgA" cells. Ensuing immune responses prevent infection of IgA B cells during later exposure to EBV at older ages. Our data implicate EBV-infected cells as the source of poorly galactosylated IgA1 in circulating immune complexes and glomerular deposits in patients with IgAN. Thus, temporal differences in EBV primo-infection as related to naturally delayed maturation of the IgA system may contribute to geographic and racial variations in incidence of IgAN.
Department of Medicine University of Alabama at Birmingham Birmingham AL United States
Department of Microbiology University of Alabama at Birmingham Birmingham AL United States
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc23004227
- 003
- CZ-PrNML
- 005
- 20230425141223.0
- 007
- ta
- 008
- 230418s2023 sz f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.3389/fimmu.2023.1085922 $2 doi
- 035 __
- $a (PubMed)36865536
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a sz
- 100 1_
- $a Mestecky, Jiri $u Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, United States $u Laboratory of Cellular and Molecular Immunology Institute of Microbiology, Czech Academy of Sciences, Prague, Czechia $u Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States
- 245 10
- $a IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease / $c J. Mestecky, BA. Julian, M. Raska
- 520 9_
- $a IgA nephropathy (IgAN) is an autoimmune disease in which poorly galactosylated IgA1 is the antigen recognized by naturally occurring anti-glycan antibodies, leading to formation of nephritogenic circulating immune complexes. Incidence of IgAN displays geographical and racial disparity: common in Europe, North America, Australia, and east Asia, uncommon in African Americans, many Asian and South American countries, Australian Aborigines, and rare in central Africa. In analyses of sera and cells from White IgAN patients, healthy controls, and African Americans, IgAN patients exhibited substantial enrichment for IgA-expressing B cells infected with Epstein-Barr virus (EBV), leading to enhanced production of poorly galactosylated IgA1. Disparities in incidence of IgAN may reflect a previously disregarded difference in the maturation of the IgA system as related to the timing of EBV infection. Compared with populations with higher incidences of IgAN, African Americans, African Blacks, and Australian Aborigines are more frequently infected with EBV during the first 1-2 years of life at the time of naturally occurring IgA deficiency when IgA cells are less numerous than in late childhood or adolescence. Therefore, in very young children EBV enters "non-IgA" cells. Ensuing immune responses prevent infection of IgA B cells during later exposure to EBV at older ages. Our data implicate EBV-infected cells as the source of poorly galactosylated IgA1 in circulating immune complexes and glomerular deposits in patients with IgAN. Thus, temporal differences in EBV primo-infection as related to naturally delayed maturation of the IgA system may contribute to geographic and racial variations in incidence of IgAN.
- 650 _2
- $a mladiství $7 D000293
- 650 _2
- $a dítě $7 D002648
- 650 _2
- $a předškolní dítě $7 D002675
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a imunokomplex $7 D000936
- 650 12
- $a infekce virem Epsteina-Barrové $x epidemiologie $x etnologie $7 D020031
- 650 12
- $a IgA nefropatie $x epidemiologie $x etnologie $7 D005922
- 650 _2
- $a virus Epsteinův-Barrové $7 D004854
- 650 _2
- $a imunoglobulin A $7 D007070
- 650 _2
- $a černoši $7 D044383
- 650 _2
- $a kojenec $7 D007223
- 651 _2
- $a Austrálie $7 D001315
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a přehledy $7 D016454
- 655 _2
- $a Research Support, N.I.H., Extramural $7 D052061
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Julian, Bruce A $u Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, United States $u Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States
- 700 1_
- $a Raska, Milan $u Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, United States $u Department of Immunology, Faculty of Medicine and Dentistry, Palacky University and University Hospital, Olomouc, Czechia
- 773 0_
- $w MED00181405 $t Frontiers in immunology $x 1664-3224 $g Roč. 14, č. - (2023), s. 1085922
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/36865536 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y p $z 0
- 990 __
- $a 20230418 $b ABA008
- 991 __
- $a 20230425141220 $b ABA008
- 999 __
- $a ok $b bmc $g 1924725 $s 1190436
- BAS __
- $a 3
- BAS __
- $a PreBMC-MEDLINE
- BMC __
- $a 2023 $b 14 $c - $d 1085922 $e 20230207 $i 1664-3224 $m Frontiers in immunology $n Front Immunol $x MED00181405
- LZP __
- $a Pubmed-20230418
