Role of Epstein-Barr Virus in Pathogenesis and Racial Distribution of IgA Nephropathy

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388971%3A_____%2F20%3A00525224" target="_blank" >RIV/61388971:_____/20:00525224 - isvavai.cz</a>

Alternative codes found

RIV/61989592:15110/20:73602945 RIV/00216208:11130/20:10410762 RIV/00098892:_____/20:N0000207 RIV/00064203:_____/20:10410762

Result on the web

<a href="https://www.frontiersin.org/articles/10.3389/fimmu.2020.00267/full" target="_blank" >https://www.frontiersin.org/articles/10.3389/fimmu.2020.00267/full</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3389/fimmu.2020.00267" target="_blank" >10.3389/fimmu.2020.00267</a>

Result language

angličtina

Original language name

Role of Epstein-Barr Virus in Pathogenesis and Racial Distribution of IgA Nephropathy

Original language description

IgA nephropathy (IgAN) is the dominant type of primary glomerulonephritis worldwide. However, IgAN rarely affects African Blacks and is uncommon in African Americans. Polymeric IgA1 with galactose-deficient hinge-region glycans is recognized as auto-antigen by glycan-specific antibodies, leading to formation of circulating immune complexes with nephritogenic consequences. Because human B cells infected in vitro with Epstein-Barr virus (EBV) secrete galactose-deficient IgA1, we examined peripheral blood B cells from adult IgAN patients, and relevant controls, for the presence of EBV and their phenotypic markers. We found that IgAN patients had more lymphoblasts/plasmablasts that were surface-positive for IgA, infected with EBV, and displayed increased expression of homing receptors for targeting the upper respiratory tract. Upon polyclonal stimulation, these cells produced more galactose-deficient IgA1 than did cells from healthy controls. Unexpectedly, in healthy African Americans, EBV was detected preferentially in surface IgM- and IgD-positive cells. Importantly, most African Blacks and African Americans acquire EBV within 2 years of birth. At that time, the IgA system is naturally deficient, manifested as low serum IgA levels and few IgA-producing cells. Consequently, EBV infects cells secreting immunoglobulins other than IgA. Our novel data implicate Epstein-Barr virus infected IgA(+) cells as the source of galactose-deficient IgA1 and basis for expression of relevant homing receptors. Moreover, the temporal sequence of racial-specific differences in Epstein-Barr virus infection as related to the naturally delayed maturation of the IgA system explains the racial disparity in the prevalence of IgAN.

Czech name

—

Czech description

—

Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

10606 - Microbiology

Project

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

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2020

Confidentiality

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

Name of the periodical

Frontiers in Immunology

ISSN

1664-3224

e-ISSN

—

Volume of the periodical

11

Issue of the periodical within the volume

FEB 28

Country of publishing house

CH - SWITZERLAND

Number of pages

15

Pages from-to

267

UT code for WoS article

000524779000001

EID of the result in the Scopus database

2-s2.0-85082081880