Anti-glomerular basement membrane antibody-induced glomerulonephritis

Wilson, Curtis B.; Dixon, Frank J.

doi:10.1038/ki.1973.14

Cited by 480 publications

(207 citation statements)

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“…Diagnosis is based on the detection of circulating autoantibodies and their deposition along the GBMs (3,4). The major autoantigen is the noncollagenous domain 1 of the a3-chain of type IV collagen (a3IV-NC1), which is targeted by both Abs and T cells (5)(6)(7).…”

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confidence: 99%

Glomerulopathy Induced by Immunization with a Peptide Derived from the Goodpasture Antigen α3IV-NC1

Hopfer

Hünemörder

Treder

et al. 2015

The Journal of Immunology

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Mouse experimental autoimmune glomerulonephritis, a model of human antiglomerular basement membrane disease, depends on both Ab and T cell responses to the Goodpasture Ag noncollagenous domain 1 of the α3-chain of type IV collagen (α3IV-NC1). The aim of our study was to further characterize the T cell–mediated immune response. Repeated immunization with mouse α3IV-NC1 caused fatal glomerulonephritis in DBA/1 mice. Although two immunizations were sufficient to generate high α3IV-NC1–specific IgG titers, Ab and complement deposition along the glomerular basement membranes, and a nephrotic syndrome, two additional immunizations were needed to induce a necrotizing/crescentic glomerulonephritis. Ten days after the first immunization, α3IV-NC1–specific CD4+ cells producing TNF-α, IFN-γ, or IL-17A were detected in the spleen. With the emergence of necrotizing/crescentic glomerulonephritis, ∼0.15% of renal CD4+ cells were specific for α3IV-NC1. Using peptides spanning the whole α3IV-NC1 domain, three immunodominant T cell epitopes were identified. Immunization with these peptides did not lead to clinical signs of experimental autoimmune glomerulonephritis or necrotizing/crescentic glomerulonephritis. However, mice immunized with one of the peptides (STVKAGDLEKIISRC) developed circulating Abs against mouse α3IV-NC1 first detected at 8 wk, and 50% of the mice showed mild proteinuria at 18–24 wk due to membranous glomerulopathy. Taken together, our results suggest that autoreactive T cells are able to induce the formation of pathologic autoantibodies. The quality and quantity of α3IV-NC1–specific Ab and T cell responses are critical for the phenotype of the glomerulonephritis.

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confidence: 99%

Glomerulopathy Induced by Immunization with a Peptide Derived from the Goodpasture Antigen α3IV-NC1

Hopfer

Hünemörder

Treder

et al. 2015

The Journal of Immunology

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“…There are some more recent reports of disease outbreaks associated with influenza virus, such as a series of four patients presenting during an influenza A2 epidemic in the early 1970s, although in these patients, confirmatory virologic or serologic evidence of infection was not shown (20). There is a small number of additional isolated patients in whom influenza infection was serologically confirmed reported in the same era (21,22). Other specific infectious associations with anti-GBM disease, however, have not been reported, and the precise mechanisms through which infection might initiate disease are not defined.…”

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confidence: 99%

Clustering of Anti-GBM Disease: Clues to an Environmental Trigger?

McAdoo

Pusey

2016

CJASN

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“…Although the pathogenic roles of anti-GBM autoantibodies against the noncollagenous domain 1 of 3 chain of type IV collagen (3(IV)NC1) have been fully demonstrated (Sado et al, 1989;Wilson and Dixon, 1973), there is strong evidence indicating that the full expression of this disease is dependent on cell-mediated autoimmunity, particular autoreactive T cells.…”

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confidence: 99%