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Cells
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Inflammation and Immune Cell Activation in Kidney Disease
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Inflammation and Immune Cell Activation in Kidney Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 9162

Special Issue Editors

Prof. Hans-Joachim Anders

E-Mail Website
Guest Editor
Nephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Munich, Germany
Interests: immunity; clinical nephrology; chronic renal failure; acute kidney injury; inflammation; innate immunity; macrophage; adaptive immunity; autoimmunity; cellular immunology
Prof. Betty Diamond

E-Mail Website
Guest Editor
Feinstein Institutes for Medical Research, Manhasset, NY, USA
Interests: B cells; autoimmunity; inflammation; neuro-immune interactions
Dr. Stefanie Steiger

E-Mail Website
Guest Editor
Division of Nephrology, Department of Medicine IV, Hospital of the Ludwig-Maximilians-University Munich, Munich, Germany
Interests: acute kidney injury; tissue repair; fibrosis; kidney stones and crystal biology; hyperuricemia; inflammation; infection; immune-cell activation and plasticity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,
Inflammation is a central pathomechanism of many forms of kidney injury and includes genetic abnormalities, e.g., of the complement systems, autoinflammation, and autoimmune conditions as a primary trigger of e.g., glomerulonephritis and renal vasculitis. However, inflammation also occurs as a secondary phenomenon in toxic or ischemic kidney injuries, frequently leading to necroinflammation or immunothrombosis leading to a wide spectrum of different lesion patterns, e.g., in thrombotic microangiopathies or tubule necrosis. In addition, inflammation is a hallmark of alloimmunity after kidney transplantation.

In contrast, alternative patterns of immune cell activation promote the healing phase upon kidney injury and therefore associate the presence of immune cells with kidney remodeling in chronic kidney disease involving the processes of persistent interstitial nephritis and fibrogenesis.

Finally, systemic inflammation contributes to the cardiovascular complications of chronic kidney disease by accelerating atherogenesis, vascular calcification, and heart failure, which produce a strong impact on the morbidity and mortality of patients with kidney disease.

This Special Issue of the journal Cells will promote the visibility of research covering these aspects of immune activation in kidney injury, kidney healing, and kidney disease-related complications.

Prof. Hans-Joachim Anders
Prof. Betty Diamond
Dr. Stefanie Steiger
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • macrophages
  • T cells
  • dendritic cells
  • cytokines
  • complement
  • biomarkers
  • necrosis
  • autoimmunity
  • transplantation

Published Papers (3 papers)

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Research

16 pages, 5328 KiB  
Article
C4d Deposition after Allogeneic Renal Transplantation in Rats Is Involved in Initial Apoptotic Cell Clearance
by Stefan Reuter, Dominik Kentrup, Alexander Grabner, Gabriele Köhler, Konrad Buscher and Bayram Edemir
Cells 2021, 10(12), 3499; https://doi.org/10.3390/cells10123499 - 10 Dec 2021
Cited by 1 | Viewed by 2306
Abstract
In the context of transplantation, complement activation is associated with poor prognosis and outcome. While complement activation in antibody-mediated rejection is well-known, less is known about complement activation in acute T cell-mediated rejection (TCMR). There is increasing evidence that complement contributes to the [...] Read more.
In the context of transplantation, complement activation is associated with poor prognosis and outcome. While complement activation in antibody-mediated rejection is well-known, less is known about complement activation in acute T cell-mediated rejection (TCMR). There is increasing evidence that complement contributes to the clearance of apoptotic debris and tissue repair. In this regard, we have analysed published human kidney biopsy transcriptome data clearly showing upregulated expression of complement factors in TCMR. To clarify whether and how the complement system is activated early during acute TCMR, experimental syngeneic and allogeneic renal transplantations were performed. Using an allogeneic rat renal transplant model, we also observed upregulation of complement factors in TCMR in contrast to healthy kidneys and isograft controls. While staining for C4d was positive, staining with a C3d antibody showed no C3d deposition. FACS analysis of blood showed the absence of alloantibodies that could have explained the C4d deposition. Gene expression pathway analysis showed upregulation of pro-apoptotic factors in TCMR, and apoptotic endothelial cells were detected by ultrastructural analysis. Monocytes/macrophages were found to bind to and phagocytise these apoptotic cells. Therefore, we conclude that early C4d deposition in TCMR may be relevant to the clearance of apoptotic cells. Full article
(This article belongs to the Special Issue Inflammation and Immune Cell Activation in Kidney Disease)
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16 pages, 5681 KiB  
Article
A Novel Treatment for Glomerular Disease: Targeting the Activated Macrophage Folate Receptor with a Trojan Horse Therapy in Rats
by Gabriela E. Garcia, Yingjuan J. Lu, Luan D. Truong, Carlos A. Roncal-Jiménez, Makoto Miyazaki, Shinobu Miyazaki-Anzai, Gabriel Cara-Fuentes, Ana Andres-Hernando, Miguel Lanaspa, Richard J. Johnson and Christopher P. Leamon
Cells 2021, 10(8), 2113; https://doi.org/10.3390/cells10082113 - 17 Aug 2021
Cited by 3 | Viewed by 2577
Abstract
Since activated macrophages express a functional folate receptor β (FRβ), targeting this macrophage population with folate-linked drugs could increase selectivity to treat inflammatory diseases. Using a macrophage-mediated anti-glomerular basement membrane (anti-GBM) glomerulonephritis (GN) in WKY rats, we investigated the effect of a novel [...] Read more.
Since activated macrophages express a functional folate receptor β (FRβ), targeting this macrophage population with folate-linked drugs could increase selectivity to treat inflammatory diseases. Using a macrophage-mediated anti-glomerular basement membrane (anti-GBM) glomerulonephritis (GN) in WKY rats, we investigated the effect of a novel folic acid-aminopterin (AMT) conjugate (EC2319) designed to intracellularly deliver AMT via the FR. We found that treatment with EC2319 significantly attenuated kidney injury and preserved renal function. Kidney protection with EC2319 was blocked by a folate competitor, indicating that its mechanism of action was specifically FRβ-mediated. Notably, treatment with methotrexate (MTX), another folic acid antagonist related to AMT, did not protect from kidney damage. EC2319 reduced glomerular and interstitial macrophage infiltration and decreased M1 macrophage recruitment but not M2 macrophages. The expression of CCL2 and the pro-fibrotic cytokine TGF-β were also reduced in nephritic glomeruli with EC2319 treatment. In EC2319-treated rats, there was a significant decrease in the deposition of collagens. In nephritic kidneys, FRβ was expressed on periglomerular macrophages and macrophages present in the crescents, but its expression was not observed in normal kidneys. These data indicate that selectively targeting the activated macrophage population could represent a novel means for treating anti-GBM GN and other acute crescentic glomerulonephritis. Full article
(This article belongs to the Special Issue Inflammation and Immune Cell Activation in Kidney Disease)
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15 pages, 5731 KiB  
Article
Immunophenotypical Characterization of M1/M2 Macrophages and Lymphocytes in Cisplatin-Induced Rat Progressive Renal Fibrosis
by Minto Nakagawa, Mohammad Rabiul Karim, Takeshi Izawa, Mitsuru Kuwamura and Jyoji Yamate
Cells 2021, 10(2), 257; https://doi.org/10.3390/cells10020257 - 28 Jan 2021
Cited by 39 | Viewed by 3544
Abstract
Renal fibrosis is regarded as the common final pathway leading to chronic kidney diseases; macrophages and myofibroblasts play important roles in the development of fibrosis. F344 rats were injected once with cisplatin (CDDP; 6 mg/kg BW) for renal lesions. Here, immunophenotypical characteristics of [...] Read more.
Renal fibrosis is regarded as the common final pathway leading to chronic kidney diseases; macrophages and myofibroblasts play important roles in the development of fibrosis. F344 rats were injected once with cisplatin (CDDP; 6 mg/kg BW) for renal lesions. Here, immunophenotypical characteristics of macrophages and lymphocytes in CDDP-induced rat renal lesions were investigated histopathologically; the CDDP-induced renal lesions consisted of tissue damage at the early-stage, worsen the damage and commencement of interstitial fibrosis at the mid-stage, and progressive fibrosis at the late stage; the KIM-1 expression and α-SMA+ myofibroblast area reflected renal tubular damage/abnormal regeneration and renal interstitial fibrosis, respectively. CD68+ M1 macrophages began to increase at the mid-stage, with increased mRNA expressions of M1-related cytokines (INF-γ, TNF-α and IL-6), and then slightly decreased at the late-stage. CD163+ M2 macrophages showed a gradually increased number at the mid- and late-stages, accompanied by increased TGF-β1 mRNA expression (a fibrogenic factor). Double immunofluorescence using fibrotic samples at the late-stage revealed that 62.0–78.0% of CD68+ M1 macrophages co-expressed CD163, indicating that M1/M2 macrophages may contribute to progressive renal fibrosis in cooperation; further, MHC class II-expressing macrophages had a tendency towards M1 polarization, whereas CD204-expressing macrophages towards M2 polarization. In addition, CD4+ and CD8+ T cells were increased at the late-stage. Collectively, progressive renal interstitial fibrosis may be developed by complicated mechanisms that arose via interaction of M1/M2 macrophages (inflammatory for M1 and anti-inflammatory for M2) and T cells reacting to CD4 (for helper) and CD8 (for cytotoxicity). This study would provide some information on the pathogenesis of renal fibrosis based on inflammatory cells. Full article
(This article belongs to the Special Issue Inflammation and Immune Cell Activation in Kidney Disease)
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