FIGURE 4.

Possible mechanisms associated with gut dysbiosis and effects of host immunity on gut microbiota in IMN patients. Alterations in the specific microbiome may be involved in the pathogenesis and development of IMN through depletion of SCFAs and sIgA, increased cytokines (TNF-α, IL-1β), uremic toxins (PCS, IS, TMAO), and common antigens (SPeB) with the glomerular basement membrane. The host immune system can regulate the gut microbiota homeostasis through the production of sIgA and the induction of Ang. IMN, idiopathic membranous nephropathy; sIgA, secretory immunoglobulin A; TMAO, trimethylamine N-oxide; PCS, p-cresol sulfate; IS, indoxyl sulfate; IL, interleukin; TNF-α, tumor necrosis factor-α; TGF-β, transforming growth factor-β; Treg, regulatory T cells; EMT, epithelial-mesenchymal transition; SPeB, streptococcal pyrogenic exotoxin B; PLA2R, phospholipase A2 receptor; THSD7A, thrombospondin type 1 domain-containing 7A; EXT1/EXT2, exostosin 1/exostosin 2; NELL-1, neural EGF-like-1 protein; Sema3B, semaphorin 3B; PCDH7, protocadherin 7; HTRA1, high-temperature requirement A serine peptidase 1; Ang, angiogenin.