I have read with keen interest the article by Cumpelik et al. (1), which presents a pioneering investigation into a novel T cell–independent pathway of B1 cell activation through anaphylatoxin-mediated secretion of BAFF by neutrophils. This compelling work has stimulated my curiosity, because I believe its implications may extend beyond the confines explored within the paper.

The pathogenesis of idiopathic nephrotic syndrome (INS) has remained an enigma for more than seven decades. Despite the description of numerous molecular mechanisms associated with INS pathogenesis, these findings remain fragmented and challenging to integrate into a cohesive framework.

A well-established facet of INS involves the dysregulated maturation and activation of B cells, characterized by the expansion of specific cellular subpopulations and the production of autoantibodies targeting the podocyte in some patients (2). Nowadays, the main proof supporting the involvement of B cells in the pathogenesis of INS is provided...

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