IL-6 and its role in IgA nephropathy development

0558971 - BTÚ 2023 RIV GB eng J - Článek v odborném periodiku
Groza, Yaroslava - Jemelková, J. - Kafkova, L. R. - Malý, Petr - Raška, M.
IL-6 and its role in IgA nephropathy development.
Cytokine & Growth Factor Reviews. Roč. 66, AUG 2022 (2022), s. 1-14. ISSN 1359-6101. E-ISSN 1879-0305
Grant CEP: GA MŠMT(CZ) EF16_025/0007397
Institucionální podpora: RVO:86652036
Klíčová slova: il-6 * IgA nephropathy * Gp130 * Galactose-deficient IgA1 (Gd-IgA1) * stat1 * stat3
Obor OECD: Biochemistry and molecular biology
Impakt faktor: 13, rok: 2022
Způsob publikování: Open access
https://www.sciencedirect.com/science/article/pii/S1359610122000235?via%3Dihub

IL-6 is considered one of the well characterized cytokines exhibiting homeostatic, pro-and anti-inflammatory activities, depending on the receptor variant and the induced intracellular cis-or trans-signaling responses. IL 6-activated pathways are involved in the regulation of cell proliferation, survival, differentiation, and cell metabolism changes.Deviations in IL-6 levels or abnormal response to IL-6 signaling are associated with several autoimmune diseases including IgA nephropathy (IgAN), one of most frequent primary glomerulonephritis worldwide. IgAN is associated with increased plasma concentration of IL-6 and increased plasma concentration of aberrantly galactosylated IgA1 immunoglobulin (Gd-IgA1). Gd-IgA1 is specifically recognized by autoantibodies, leading to the formation of circulating immune complexes (CIC) with nephritogenic potential, since CIC deposited in the glomerular mesangium induce mesangial cells proliferation and glomerular injury. Infection of the upper respiratory or digestive tract enhances IL-6 production and in IgAN patients is often followed by the macroscopic hematuria.This review recapitulates general aspects of IL-6 signaling and summarizes experimental evidences about IL-6 involvement in the etiopathogenesis of IgA nephropathy through the production of Gd-IgA1 and regulation of mesangial cell proliferation.
Trvalý link: https://hdl.handle.net/11104/0333059