2020
DOI: 10.3389/fimmu.2020.01846
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Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity

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Cited by 30 publications
(24 citation statements)
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References 119 publications
(158 reference statements)
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“…Th17 cells in IMN have been a heated topic recently, and studies from different research groups suggested the up-regulation of Th17 and the increase of IL-6 and IL-17A. This indicates that IMN is conducive to Th17 cells differentiation, and also strengthens our confidence that IMN is originated from extrarenal inflammation (115). Increased Th17 cells are also associated with a higher recurrence rate and a higher risk of venous thrombosis (71), which is a concern for clinical treatment.…”
Section: Th Cells Involved In the Immune Dysregulation Of Imnmentioning
confidence: 78%
See 1 more Smart Citation
“…Th17 cells in IMN have been a heated topic recently, and studies from different research groups suggested the up-regulation of Th17 and the increase of IL-6 and IL-17A. This indicates that IMN is conducive to Th17 cells differentiation, and also strengthens our confidence that IMN is originated from extrarenal inflammation (115). Increased Th17 cells are also associated with a higher recurrence rate and a higher risk of venous thrombosis (71), which is a concern for clinical treatment.…”
Section: Th Cells Involved In the Immune Dysregulation Of Imnmentioning
confidence: 78%
“…Cellular immune-mediated diseases are usually infiltrated by local monocytes and cytotoxic T cells. Although IMN presents as an organ-specific autoimmune disease, there is a local lack of cell infiltration that mediates cellular immunity in the glomerulus, and the generation of proteinuria may be caused by antibody activation of complement that damages the podocytes or antibody affecting podocyte function (115)(116)(117). The predictive value of anti-PLA2R antibody titers for clinical prognosis has also been vigorously described (69).…”
Section: Th Cells Involved In the Immune Dysregulation Of Imnmentioning
confidence: 99%
“…Podocytes are epithelial cells of the glomerular viscera, located outside the glomerular basement membrane, and autoantibodies bind to antigens on the surface of podocytes, forming an in situ immune complex that results in disease ( 2 , 5 ). In situ immune complexes differ from circulating immune complexes in that they do not come into contact with circulating inflammatory mediators and generally do not trigger inflammatory reactions ( 7 ). Therefore, they are more likely to trigger podocyte lesion formation by activating complement, leading to proteinuria and renal tissue damage ( 8 ).…”
Section: Introductionmentioning
confidence: 99%
“…This association between PLA2R autoantibodies and disease activity suggests that the monitoring and quantification of autoantibodies may be for therapy in patients with MN and a valuable tool for determining treatment strategies. In addition to PLA2R, podocyte biomarkers identified in patients with IMN include neural epidermal growth factor-like 1 protein (NELL-1) and thrombospondin type-1 domain-containing 7A (THSD7A), accounting for 5–10% and 3–5% of adult IMN, respectively 15 . Currently, only serum anti-PLA2R antibody detection is widely used in guiding the IMN clinical diagnosis, prognosis, and treatment of IMN.…”
Section: Introductionmentioning
confidence: 99%