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Abstract

Minimal change nephrotic syndrome (MCNS) is the most common cause of nephrotic syndrome in children and accounts for 10–25 % of nephrotic syndrome in adults. The etiology has been postulated as T lymphocytes (T cell) disorder; however, precise mechanisms still remain unknown. CD80 (also known as B7.1) is a transmembrane glycoprotein which is usually expressed on antigen-presenting cells (APC) and acts as a co-stimulatory signal for T cell activation. The role of CD80 expression in podocytes as a cause of proteinuric condition was first described by Reiser et al. in 2004. Administration of lipopolysaccharides (LPS) and puromycin aminonucleoside, knockout of alpha-3 integrin, and lupus nephritis were associated with CD80 induction in podocytes and concomitant proteinuria. Besides, LPS-induced proteinuria was not observed in CD80 knockout mice. In 2009, Garin et al. demonstrated that urinary CD80 levels are elevated in MCNS in relapse compared with those observed in remission and control subjects. Importantly, elevated urinary CD80 was suggested as a possible biomarker to distinguish MCNS and focal segmental glomerulosclerosis. Besides, polyinosinic:polycytidylic acid (polyI:C), ligand of Toll-like receptor 3 which mimics viral infection, induced CD80 in the podocytes. Thus, it is a possible explanation for the frequent relapses of MCNS after upper respiratory virus infections. LPS and polyI:C only induced transient proteinuria; therefore, impaired regulatory mechanisms after CD80 induction were postulated as a second hit cause of MCNS.

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Shimada, M., Ishimoto, T., Johnson, R.J. (2016). Co-stimulatory Molecule CD80 (B7.1) in MCNS. In: Kaneko, K. (eds) Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55270-3_4

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