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Role of IgG autoantibodies in the pathogenesis of IgA nephropathy assessed in a passive mouse model

ABSTRACT: Role of IgG autoantibodies in the pathogenesis of IgA nephropathy assessed in a passive mouse model

PROVIDER: PRJNA657001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12446926.fastq.gz	Fastqsanger.gz
	SRR12446927.fastq.gz	Fastqsanger.gz
	SRR12446928.fastq.gz	Fastqsanger.gz
	SRR12446929.fastq.gz	Fastqsanger.gz

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Role of IgG autoantibodies in the pathogenesis of IgA nephropathy assessed in a passive mouse model

Project description:IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, is characterized by IgA1-containing glomerular immunodeposits. These immunodeposits are thought to originate from the circulating immune complexes consisting of aberrantly glycosylated IgA1 (galactose-deficient IgA1; Gd-IgA1) bound by IgG autoantibodies. This hypothesis is supported by the findings that renal immunodeposits of IgA nephropathy patients are enriched for IgG autoantibodies specific for galactose-deficient IgA1 (Rizk et al., J. Am. Soc. Nephrol. 30(10), 2017-2026, 2019). However, experimental proof is needed. This study provides in vivo data in mice that support the pathogenic role of IgG autoantibodies in IgAN.

2021-01-31 | GSE156179 | GEO

Lupus IgA1 autoantibodies synergize with IgG to enhance pDC responses to RNA-containing immune complexes

Project description:Autoantibodies to nuclear antigens are hallmarks for diagnosis of the autoimmune disease systemic lupus erythematosus (SLE) and they contribute to SLE pathogenesis. However, there remains a gap in our knowledge regarding how different isotypes of autoantibodies contribute to key disease processes, including the production of the critical type I interferon (IFN) cytokines by plasmacytoid dendritic cells (pDCs) in response to immune complexes (ICs). Here, we show that individuals with SLE have IgA autoantibodies against most nuclear antigens assessed, largely correlating with the amounts of IgG against the same antigen. We investigated whether IgA autoantibodies against a major SLE autoantigen, Smith ribonucleoproteins (Sm/RNPs), play a role in IC activation of pDCs. We found that pDCs express the IgA-specific Fc receptor, FcRI, and there was a striking ability of IgA1 isotype autoantibodies to synergize with IgG in RNA-containing ICs to generate robust pDC IFN responses. pDC responses to these ICs required both FcRI and FcRIIa, suggesting the most potent ICs for pDCs contained autoantibodies of both isotypes. Sm/RNP IC binding to and internalization by pDCs were greater when ICs contained both IgA1 and IgG. In addition, binding of Sm/RNP ICs generated with IgA1-sufficient serum correlated to pDC FcRI expression, but not FcRIIa expression. pDCs from individuals with SLE had higher binding of IgA1-containing ICs and higher expression of FcRI than pDCs from healthy control individuals, correlating with expression of IFN response genes. Taken together, our data indicate that IgA1 ANAs contribute to SLE pathology and warrant further investigation.

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New-Onset IgG Autoantibodies in Hospitalized Patients with COVID-19 [viral]

Project description:We developed three different protein arrays to measure IgG autoantibodies associated with Connective Tissue Diseases (CTDs), Anti-Cytokine Antibodies (ACA), and anti-viral antibody responses in 147 hospitalized COVID-19 patients in three different centers.

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New-Onset IgG Autoantibodies in Hospitalized Patients with COVID-19

Project description:New-Onset IgG Autoantibodies in Hospitalized Patients with COVID-19

| PRJNA749308 | ENA

Galactose-deficient IgA1 and the corresponding IgG autoantibodies predict IgA nephropathy progression.

Project description:BackgroundIgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, has serious outcomes with end-stage renal disease developing in 30-50% of patients. The diagnosis requires renal biopsy. Due to its inherent risks, non-invasive approaches are needed.MethodsWe evaluated 91 Czech patients with biopsy-proven IgAN who were assessed at time of diagnosis for estimated glomerular filtration rate (eGFR), proteinuria, microscopic hematuria, and hypertension, and then followed prospectively. Serum samples collected at diagnosis were analyzed for galactose-deficient IgA1 (Gd-IgA1) using new native-IgA1 and established neuraminidase-treated-IgA1 tests, Gd-IgA1-specific IgG autoantibodies, discriminant analysis and logistic regression model assessed correlations with renal function and Oxford classification (MEST score).ResultsSerum levels of native (P <0.005) and neuraminidase-treated (P <0.005) Gd-IgA1 were associated with the rate of eGFR decline. A higher relative degree of galactose deficiency in native serum IgA1 predicted a faster eGFR decline and poor renal survival (P <0.005). However, Gd-IgA1 has not differentiated patients with low vs. high baseline eGFR. Furthermore, patients with high baseline eGFR that was maintained during follow-up were characterized by low serum levels of Gd-IgA1-specific IgG autoantibodies (P = 0.003).ConclusionsIncluding levels of native and neuraminidase-treated Gd-IgA1 and Gd-IgA1-specific autoantibodies at diagnosis may aid in the prognostication of disease progression in Czech patients with IgAN. Future tests will assess utility of these biomarkers in larger patients cohorts from geographically distinct areas.

| S-EPMC6386256 | biostudies-literature

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