Description
IgA nephropathy (IgAN) is an autoimmune disorder with a partially understood cause. It is the most prevalent form of primary glomerulonephritis and a common contributor to end-stage renal disease. The pathogenesis of IgAN is explained by the multi-hit model, which combines findings from studies of IgAN patients. This model highlights several key processes: the increased production of aberrantly glycosylated galactose-deficient IgA1 (GdIgA1, hit 1), the formation of antibodies against GdIgA1 (hit 2), the development of immune complexes (hit 3), and the mechanisms by which these immune complexes cause kidney damage (hit 4). Although B cells are central to producing these pathogenic antibodies, they are not included in the multi-hit model. Moreover, there are significant gaps in understanding the activation and differentiation pathways of B cells that lead to the secretion of harmful IgA antibodies in IgAN. This knowledge gap hinders the development of effective immunosuppressive treatments for the condition. Recent findings on budesonide highlight the importance of mucosal immunity in disease activity, which may be attributed to B cells within mucosa-associated lymphatic tissue. Our next project “Unveiling molecular determinants and developmental niches for GdIgA+ B cell differentiation in IgA nephropathy” aims to unravel these complexities by targeting mucosal immune regulation, with the hope of opening new doors for treatment strategies.| Period | 4 Oct 2024 |
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| Event title | XVII Baltic Nephrology Conference |
| Event type | Conference |
| Conference number | 17 |
| Location | Tartu, EstoniaShow on map |
| Degree of Recognition | International |