Immune-mediated glomerular diseases: new basic concepts and clinical implications

Panzer, Ulf; Huber, Tobias B.

doi:10.1007/s00441-021-03509-5

Cited by 4 publications

(3 citation statements)

References 17 publications

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“…Usually, p-ANCA vasculitis surfaces several years later, and infections can trigger the autoimmunity. However, limited literature is available to entertain the potential immunemediated mechanisms resulting in various types of glomerular pathology, presentation, and treatment variabilities [6]. A prevalence of 21% of the overlap syndrome of RA and p-ANCA-vasculitis have been reported [7].…”

Section: Discussionmentioning

confidence: 99%

Antineutrophil Cytoplasmic Antibody (ANCA)-Associated Renal Vasculitis After COVID-19 Infection: A Case Report

Kataria¹,

Rogers²,

Sadia³

et al. 2022

Cureus

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Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a class of autoimmune diseases that can cause kidney failure because of mononuclear cell infiltration and the destruction of small and mediumsized blood vessels. Coronavirus disease 2019 (COVID-19) may trigger or exacerbate autoimmune diseases. We present a case of ANCA-associated vasculitis in a patient with rheumatoid arthritis after a COVID-19 infection, who presented with intermittent hemoptysis and dyspnea and was diagnosed with COVID-19 pneumonia three weeks ago. Her clinical, radiological, and serological picture was concerned with pulmonary-renal syndrome. Her serum was positive for antinuclear antibody and ANCAs, and renal biopsy showed pauci-immune crescentic glomerulonephritis. She was diagnosed clinicopathologically with pauciimmune glomerulonephritis in the setting of rheumatoid arthritis (RA) after a COVID-19 infection. Her condition improved after she was treated with rituximab and pulse dose methylprednisolone.

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Section: Discussionmentioning

confidence: 99%

Antineutrophil Cytoplasmic Antibody (ANCA)-Associated Renal Vasculitis After COVID-19 Infection: A Case Report

Kataria¹,

Rogers²,

Sadia³

et al. 2022

Cureus

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“…Therefore, TLRs are often reported in the literature as a kind of threat sensors promoting the activation of not only cells of the immune system, but also internal kidney cells (podocytes). These cells are constantly exposed not only to many different compounds dissolved in the plasma, but also to the other dangers resulting from their unique location in the renal glomeruli [ 22 , 23 ]. Research to date on the role of TLR9in the pathogenesis of kidney disease is relatively scarce and focuses on acute kidney injury (AKI), chronic kidney disease (CKD) [ 24 ], systemic lupus erythematosus (SLE) [ 25 ], diabetic nephropathy [ 26 ] IgAN [ 27 ], and MPGN [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

The Importance of Toll-like Receptor 9 Expression on Monocytes and Dendritic Cells in the Context of Epstein–Barr Virus Infection in the Immunopathogenesis of Primary Glomerulonephritis

Smarz-Widelska¹,

Mertowski

Mertowska

et al. 2022

IJMS

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Toll-like receptor 9 (TLR9) is activated by unmethylated cytosine-phosphate-guanosine (CpG) dinucleotides found in the genomes of pathogens such as Epstein–Barr virus (EBV). The aim of this study was to determine the role of TLR9 in the immunopathogenesis of IgA nephropathy (IgAN) and membranoproliferative glomerulonephritis (MPGN) in the context of Epstein–Barr virus (EBV) infection. For this purpose, the frequency of TLR9-positive monocytes and dendritic cells (DCs, i.e., BDCA-1; myeloid dendritic cells, and BDCA-2; plasmocytoid dendritic cells) was studied, and a quantitative analysis of the concentration of TLR9 in the serum of patients diagnosed with IgAN and MPGN was undertaken. Higher frequencies of TLR9-positive DCs and monocytes in IgAN and MPGN patients were observed as compared with the control group. Patients diagnosed with GN exhibited a higher percentage of BDCA-1+CD19− and BDCA-2+CD123+ DCs than patients in the control group. Moreover, serum TLR9 concentration was shown to be significantly correlated with EBV DNA copy number/µg DNA, IgG, IgM, serum albumin, total protein in 24-h urine collection test and the frequency of BDCA-2+CD123+ DCs in peripheral blood. Our findings confirm that TLR9 may be involved in the development of IgAN and MPGN.

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“…Whereas renal inflammation can initially result from diverse causative factors, such as systemic immunemediated diseases, e.g., antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis and systemic lupus erythematosus, or kidney-restricted diseases, e.g., immunoglobulin A nephropathy [1][2][3], the recruitment of immune cells into the kidney is a histopathological feature shared by this group of diseases and is correlated to their clinical course [2,4]. In the majority of cases, though, personalized treatment strategies are yet impeded by the lack of comprehensively understanding the underlying molecular inflammatory pathways [5].…”

Section: Introductionmentioning

confidence: 99%

Targeting Monocyte Derived CCL17 Attenuates Murine Crescentic Glomerulonephritis by Affecting Renal CCR4<sup>+</sup> Regulatory T-Cell Recruitment

Song,

Paust,

Asada

et al. 2023

Am J Nephrol

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Introduction: The chemokine receptor CCR4 is expressed by divers CD4+ T cell subsets including regulatory T cells (Tregs) but its functional importance for leukocyte recruitment and the relevance of its two corresponding chemokines CCL17 and CCL22 have not been studied in immune mediated crescentic glomerulonephritis (cGN). Methods: Utilizing the single cell RNA sequencing (scRNAseq) data in analyzing leukocytes isolated from both human and murine nephritic kidneys we identified CCL17 as a potential therapeutic target in immune mediated renal disease. Using a mouse model of murine cGN we then delineated the effects of targeting CCL17 by neutralizing antibodies and in Ccl17 gene-deficient mice. Results: Unsupervised scRNAseq analyses identified the CCL17-CCR4 axis as a mechanism potentially involved in renal T cell migration. Analyses of functional kidney impairment and histopathological kidney damage revealed an attenuation of crescentic GN in anti-CCL17 antibody-treated mice which was corroborated using in Ccl17 gene-deficient mice. Immunohistochemical analyses revealed that these changes were accompanied by an affected renal Treg recruitment in both experimental approaches. Conclusion: The chemokine receptor CCR4 and its corresponding chemokine CCL17 are expressed in human and murine cGN and targeting the CCR4-CCL17 axis by neutralizing antibodies as well as Ccl17 gene-deficiency led to increased renal Treg recruitment and reduced histological and functional kidney damage in murine crescentic glomerulonephritis.

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Immune-mediated glomerular diseases: new basic concepts and clinical implications

Abstract: Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Cited by 4 publications

References 17 publications

Antineutrophil Cytoplasmic Antibody (ANCA)-Associated Renal Vasculitis After COVID-19 Infection: A Case Report

Antineutrophil Cytoplasmic Antibody (ANCA)-Associated Renal Vasculitis After COVID-19 Infection: A Case Report

The Importance of Toll-like Receptor 9 Expression on Monocytes and Dendritic Cells in the Context of Epstein–Barr Virus Infection in the Immunopathogenesis of Primary Glomerulonephritis

Targeting Monocyte Derived CCL17 Attenuates Murine Crescentic Glomerulonephritis by Affecting Renal CCR4<sup>+</sup> Regulatory T-Cell Recruitment

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