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IgG Glycosylation-Dependent CLEC7A Signaling Drives Podocyte Dysfunction in Lupus Nephritis
DOI:10.1002/art.70260.png)
Abstract
En 中文
Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus (SLE) that can lead to end-stage kidney disease and increased mortality. Immunoglobulin G (IgG) from LN patients displays abnormal glycosylation, contributing to podocyte injury. CLEC7A (C-type lectin domain family 7 member A) is a transmembrane lectin receptor that recognizes fucose on IgG. This study investigates the role of lectin-glycan interactions in LN-related podocyte dysfunction.
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