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Nat. Rev. Nephrol. doi:10.1038/nrneph.2015.208 Figure 1 Mechanisms of normal IgA production in the mucosal and systemic arms of the IgA immune system in humans Figure 1 | Mechanisms of normal IgA production in the mucosal and systemic arms of the IgA immune system in humans. Immunocompetent primed B cells are produced in inductive sites and migrate to the mucosal lamina propria where they mature into IgA-secreting plasma cells. These plasma cells release dimeric IgA1 or IgA2, which can bind to other IgA molecules of the same class, forming dimeric IgA (dIgA) or larger polymeric IgA (pIgA) proteins. dIgA or pIgA bind to the polymeric immunoglobulin receptor (pIgR) on the basolateral surface of the mucosal epithelium and undergo transcytosis to the apical surface where they detach from the pIgR but take with them the secretory component of the receptor. The pIgA molecule with the secretory compartment attached is known as secretory IgA (sIgA). The majority of the IgA that reaches the circulation is synthesized in the bone marrow, predominantly in a monomeric form (mIgA1). APRIL, tumour necrosis factor ligand superfamily member 13; BAFF, tumour necrosis factor ligand superfamily member 13B; BALT, bronchial-associated lymphoid tissue; GALT, gut-associated lymphoid tissue; MALT, mucosal-associated lymphoid tissue; TGF-β transforming growth factor β. Floege, J. & Feehally, J. (2015) The mucosa–kidney axis in IgA nephropathy Nat. Rev. Nephrol. doi:10.1038/nrneph.2015.208