IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease

0571660 - MBÚ 2024 RIV CH eng J - Článek v odborném periodiku
Městecký, Jiří - Julian, Bruce A. A. - Raška, M.
IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease.
Frontiers in Immunology. Roč. 14, 7 February (2023), č. článku 1085922. ISSN 1664-3224. E-ISSN 1664-3224
Institucionální podpora: RVO:61388971
Klíčová slova: IgA nephropathy * Epstein-Barr virus * galactose-deficient IgA1 * IgA system maturation * age of infection * virus spread
Obor OECD: Microbiology
Impakt faktor: 7.3, rok: 2022
Způsob publikování: Open access
https://www.frontiersin.org/articles/10.3389/fimmu.2023.1085922/full

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.
Trvalý link: https://hdl.handle.net/11104/0342863