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Editorial
. 2022 May;33(5):873-875.
doi: 10.1681/ASN.2022020201. Epub 2022 Apr 7.

Further Evidence for the Mucosal Origin of Pathogenic IgA in IgA Nephropathy

Chee Kay Cheung  1   2 , Jonathan Barratt  1   2
Affiliations
Editorial

Further Evidence for the Mucosal Origin of Pathogenic IgA in IgA Nephropathy

Chee Kay Cheung et al. J Am Soc Nephrol. 2022 May.
No abstract available

Keywords: B cells; IgA; IgA nephropathy; galactose-deficient IgA1; immunoglobulin A; immunology; lambda light chains.

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Figures

Figure 1.
Figure 1.
The mucosal immune system plays a key role in the production of GdIgA1 in IgA nephropathy. MALT represents key antigen sampling and inductive sites, and important interactions in IgAN are depicted here. Antigens are taken up by intestinal M cells and, subsequently, by dendritic cells (DC). After priming by DC, naive CD4+ T cells differentiate into T helper cells. T follicular helper (Tfh) cells interact with naive B cells, which undergo class switching to form IgA+ B cells. T cell–independent class switching also occurs through interaction of DC with naive B cells. These processes are promoted by factors including B-cell activating factor (BAFF) and APRIL. IgA+ cells then leave the MALT and enter into the lymphatic system and circulation, on their way to effector sites. Zachova et al. demonstrate increased levels of GdIgA1+ λ+ B cells in the circulation that express gut (CCR9) or respiratory tract (CCR10) homing receptors in patients with IgAN. GdIgA1+ λ+ B cells may then traffic to these sites where IgA is secreted. In IgAN, increased levels of circulating GdIgA1 are found, which may be produced by spillover, from mucosal sites or from B cells that have mishomed to systemic sites, such as the bone marrow. This leads to the formation of IgA1 immune complexes, which subsequently deposit within the glomerular mesangium. Dotted lines represent putative pathways.
See this image and copyright information in PMC

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References

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