New avian model of experimental glomerulonephritis consistent with mediation by cellular immunity. Nonhumorally mediated glomerulonephritis in chickens.

Bolton, W. Kline; Tucker, F L; Sturgill, Benjamin C.

doi:10.1172/jci111328

Cited by 113 publications

(91 citation statements)

References 33 publications

(27 reference statements)

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“…For measurement of IFN-␥ mRNA by real-time PCR, 1 g of RNA (n ϭ 6 to 7 for each group with GN) was treated with 1 unit of amplification-grade DNase I (Invitrogen) then primed with 500 ng of Oligo(dT) [12][13][14][15][16][17][18] (Roche, Mannheim, Germany) and reverse transcribed (Super Script II; Invitrogen). Gene-specific primers for murine IFN-␥ and murine ␤-actin were designed (Vector NTI software; Invitrogen).…”

Section: Assessment Of Il-18 In Nephritic Kidneysmentioning

confidence: 99%

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IL-12p40 and IL-18 in Crescentic Glomerulonephritis

Kitching

Turner

Wilson

et al. 2005

Journal of the American Society of Nephrology

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Section: Assessment Of Il-18 In Nephritic Kidneysmentioning

confidence: 99%

“…Severe crescentic glomerular injury is Th1 directed, effector CD4ϩ cell mediated (6,7), and regulated by endogenous and exogenous Th2 cytokines IL-4 and IL-10 (8 -10). Although it is clear that humoral immune mediators are capable of inducing injury (11,12), crescent formation can occur in the absence of autologous antibody (13)(14)(15).…”

mentioning

confidence: 99%

IL-12p40 and IL-18 in Crescentic Glomerulonephritis

Kitching

Turner

Wilson

et al. 2005

Journal of the American Society of Nephrology

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“…After deposition of rabbit gammaglobulin in rat glomeruli, adoptive transfer of antigen-specific syngeneic T cells can elicit GN. 2 Bolton et al, 4 using neonatally bursectomized chickens, also directly demonstrated a role for cell-mediated immunity in the development of nephritis. Most recently, Radeke et al 10 demonstrated that appropriate phenotypes of clonotypic T cells can elicit proteinuria in immunodeficient mice, if specific antigen accumulates within the glomerular mesangium prior to the adoptive transfer of the effector/memory cells.…”

mentioning

confidence: 99%

“…[1][2][3][4][5][6][7][8][9][10] T cells clearly modulate antibody responses to T-dependent antigens, and the resulting antibodies can contribute to immune complex-mediated glomerulonephritis (GN). 1,2 Moreover, Tipping et al 8 reported that macrophage accumulation in experimental anti-glomerular basement membrane antibodyinduced GN is preceded by T-cell accumulation.…”

mentioning

confidence: 99%

Development of immune-complex glomerulonephritis in athymic mice: T cells are not required for the genesis of glomerular injury

Bagheri

Pepple

Hassan

et al. 2005

Laboratory Investigation

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Chronic injection of dextran into normal mice elicits a glomerulonephritis (GN) that models IgA nephropathy (IgAN) in humans. Since athymic mice lack T cells but nonetheless develop antibodies to polysaccharide antigens such as dextran (DEX), we used athymic mice to study the role of T lymphocytes in the induction of this form of GN, independent of the role of T cells in antibody synthesis. Both mice given injections of diethylaminoethyl (DEAE)-DEX and uninjected mice had circulating IgM and IgA anti-DEX antibodies, which apparently arise as 'natural antibodies,' but immune complex GN was observed only in the injected mice. All of 15 injected mice exhibited capillary staining for IgA and IgM; none of 12 control mice contained such IgA deposits and only one had capillary staining for IgM (both Po0.001). In addition, IgG and C3 were detected in injected but not control animals. By light microscopy, injected mice exhibited marked expansion of mesangial matrix relative to controls. Electron microscopy showed no glomerular abnormalities in control mice, whereas injected mice showed large organized fibrillar deposits principally in the mesangium. Hematuria and proteinuria were present in all 15 injected mice, but only one of 11 control mice showed hematuria or proteinuria (both Po0.001). These results indicate that chronic injection of DEAE-DEX into athymic mice generates the same clinical and histologic features of GN as in euthymic mice, suggesting that T cells are not necessary to promote GN in this model.

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“…Anti-GBM GN has been studied in a number of animal models using immunizations with heterologous or homologous GBM preparations or a3IV-NC1 to breach tolerance against the autoantigen, often referred to as experimental autoimmune GN (EAG) (10)(11)(12)(13). We have previously characterized the T cell response to heterologous human a3IV-NC1 in DBA/1 mice and found a biphasic disease course.…”

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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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New avian model of experimental glomerulonephritis consistent with mediation by cellular immunity. Nonhumorally mediated glomerulonephritis in chickens.

Abstract: Astract. The present study examined the role of cell-mediated immunity (CMI)

Cited by 113 publications

References 33 publications

IL-12p40 and IL-18 in Crescentic Glomerulonephritis

IL-12p40 and IL-18 in Crescentic Glomerulonephritis

Development of immune-complex glomerulonephritis in athymic mice: T cells are not required for the genesis of glomerular injury

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

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