Gross, Oliver

[["dc.bibliographiccitation.firstpage","76"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.lastpage","83"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Andersen, Kirstin"],["dc.contributor.author","Kesper, Marie Sophie"],["dc.contributor.author","Marschner, Julian A."],["dc.contributor.author","Konrad, Lukas"],["dc.contributor.author","Ryu, Mi"],["dc.contributor.author","Kumar VR, Santhosh"],["dc.contributor.author","Kulkarni, Onkar P."],["dc.contributor.author","Mulay, Shrikant R."],["dc.contributor.author","Romoli, Simone"],["dc.contributor.author","Demleitner, Jana"],["dc.contributor.author","Schiller, Patrick"],["dc.contributor.author","Dietrich, Alexander"],["dc.contributor.author","Müller, Susanna"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Ruscheweyh, Hans-Joachim"],["dc.contributor.author","Huson, Daniel H."],["dc.contributor.author","Stecher, Bärbel"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.date.accessioned","2020-12-10T18:42:47Z"],["dc.date.available","2020-12-10T18:42:47Z"],["dc.date.issued","2017"],["dc.description.abstract","CKD associates with systemic inflammation, but the underlying cause is unknown. Here, we investigated the involvement of intestinal microbiota. We report that collagen type 4 alpha 3-deficient mice with Alport syndrome related progressive CKD displayed systemic inflammation, including increased plasma levels of pentraxin-2 and activated antigen presenting cells, CD4 and CD8 T cells, and Th17 or IFN gamma-producing T cells in the spleen as well as regulatory T cell suppression. CKD related systemic inflammation in these mice associated with intestinal dysbiosis of proteobacterial blooms, translocation of living bacteria across the intestinal barrier into the liver, and increased serum levels of bacterial endotoxin. Uremia did not affect secretory IgA release into the ileum lumen or mucosal leukocyte subsets. To test for causation between dysbiosis and systemic inflammation in CKD, we eradicated facultative anaerobic microbiota with antibiotics. This eradication prevented bacterial translocation, significantly reduced serum endotoxin levels, and fully reversed all markers of systemic inflammation to the level of nonuremic controls. Therefore, we conclude that uremia associates with intestinal dysbiosis, intestinal barrier dysfunction, and bacterial trans location, which trigger the state of persistent systemic inflammation in CKD. Uremic dysbiosis and intestinal barrier dysfunction may be novel therapeutic targets for intervention to suppress CKD related systemic inflammation and its consequences."],["dc.identifier.doi","10.1681/ASN.2015111285"],["dc.identifier.eissn","1533-3450"],["dc.identifier.isi","000391647700012"],["dc.identifier.issn","1046-6673"],["dc.identifier.pmid","27151924"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78080"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Soc Nephrology"],["dc.relation.issn","1533-3450"],["dc.relation.issn","1046-6673"],["dc.title","Intestinal Dysbiosis, Barrier Dysfunction, and Bacterial Translocation Account for CKD–Related Systemic Inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","482"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","494"],["dc.bibliographiccitation.volume","228"],["dc.contributor.author","Ryu, M. I."],["dc.contributor.author","Migliorini, Adriana"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Shankland, Stuart"],["dc.contributor.author","Brinkkoetter, Paul T."],["dc.contributor.author","Hagmann, Henning"],["dc.contributor.author","Romagnani, Paola"],["dc.contributor.author","Liapis, Helen"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.date.accessioned","2018-11-07T09:02:32Z"],["dc.date.available","2018-11-07T09:02:32Z"],["dc.date.issued","2012"],["dc.description.abstract","Glomerular crescents are most common in rapidly progressive glomerulonephritis but also occur in noninflammatory chronic glomerulopathies; thus, factors other than inflammation should trigger crescent formation, eg vascular damage and plasma leakage. Here we report that Alport nephropathy in Col4A3-deficient Sv129 mice is complicated by diffuse and global crescent formation in which proliferating parietal epithelial cells are the predominant cell type. Laminin staining and transmission and acellular scanning electron microscopy of acellular glomeruli documented disruptions and progressive disintegration of the glomerular basement membrane in Col4A3-deficient mice. FITC-dextran perfusion further revealed vascular leakage from glomerular capillaries into Bowman's space, further documented by fibrin deposits in the segmental crescents. Its pathogenic role was validated by showing that the fibrinolytic activity of recombinant urokinase partially prevented crescent formation. In addition, in vitro studies confirmed an additional mitogenic potential of serum on murine and human parietal epithelial cells. Furthermore, loss of parietal cell polarity and unpolarized secretion of extracellular matrix components were evident within fibrocellular crescents. Among 665 human Alport nephropathy biopsies, crescent formation was noted in 0.4%. We conclude that glomerular vascular injury and GBM breaks cause plasma leakage which triggers a wound healing programme involving the proliferation of parietal cells and their loss of polarity. This process can trigger cellular and fibrocellular crescent formation even in the absence of cellular inflammation and rupture of the Bowman's capsule. Copyright (C) 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.4046"],["dc.identifier.isi","000313949800007"],["dc.identifier.pmid","22553158"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24705"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0022-3417"],["dc.title","Plasma leakage through glomerular basement membrane ruptures triggers the proliferation of parietal epithelial cells and crescent formation in non-inflammatory glomerular injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","40"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","47"],["dc.bibliographiccitation.volume","218"],["dc.contributor.author","Clauss, Sebastian"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Kulkarni, Onkar"],["dc.contributor.author","Avila-Ferrufino, Alejandro"],["dc.contributor.author","Radomska, Ewa"],["dc.contributor.author","Segerer, Stephan"],["dc.contributor.author","Eulberg, Dirk"],["dc.contributor.author","Klussmann, Sven"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.date.accessioned","2018-11-07T08:30:24Z"],["dc.date.available","2018-11-07T08:30:24Z"],["dc.date.issued","2009"],["dc.description.abstract","Lack of the alpha 3 or alpha 4 chain of type IV collagen (COL4) causes autosomal recessive Alport nephropathy in humans and mice that is characterized by progressive glomerulosclerosis and tubulointerstitial disease. Renal pathology is associated with chemokine-mediated macrophage infiltrates but their contribution to the progression of Alport nephropathy is unclear. We found Ccl2 to be expressed in increasing amounts during the progression of nephropathy in Col4a3-deficient mice; hence, we blocked Ccl2 with anti-Ccl2 Spiegelmers, biostable L-enantiomeric RNA aptamers suitable for in vivo applications. Ccl2 blockade reduced the recruitment of ex vivo-labelled macrophages into kidneys of Col4a3-deficient mice. We therefore hypothesized that a prolonged course of Ccl2 blockade would reduce renal macrophage counts and prevent renal pathology in Col4a3-deficient mice. Groups of Col4a3-deficient mice received subcutaneous injections of either an anti-mCcl2 Spiegelmer or non-functional control Spiegelmer on alternate days, starting from day 21 or 42 of age. Glomerular and interstitial macrophage counts were found to be reduced with Ccl2 blockade by 50% and 30%, respectively. However, this was not associated with an improvement of glomerular pathology, interstitial pathology, or of overall survival of Col4a3-deficient mice. We conclude that Ccl2 mediates the recruitment of glomerular and interstitial macrophages but this mechanism does not contribute to the progression of Alport nephropathy in Col4a3-deficient mice. Copyright (C) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.2505"],["dc.identifier.isi","000265546200004"],["dc.identifier.pmid","19156777"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16888"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","John Wiley & Sons Ltd"],["dc.relation.issn","0022-3417"],["dc.title","Ccl2/Mcp-1 blockade reduces glomerular and interstitial macrophages but does not ameliorate renal pathology in collagen4A3-deficient mice with autosomal recessive Alport nephropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","189"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","198"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Ryu, M. I."],["dc.contributor.author","Kulkarni, Onkar"],["dc.contributor.author","Radomska, Ewa"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.date.accessioned","2018-11-07T09:01:38Z"],["dc.date.available","2018-11-07T09:01:38Z"],["dc.date.issued","2011"],["dc.description.abstract","Loss of function mutations in the alpha 3 or alpha 4 chain of type IV collagen cause Alport nephropathy, characterized by progressive glomerulosclerosis. While studying the mechanisms that determine disease progression, we found that the evolution of kidney disease in Col4a3-deficient mice was associated with an influx of immune cell subsets including nonactivated macrophages. This suggested that intrarenal inflammation might accelerate Alport nephropathy. A possible mechanism might be the well-known enhancement of immune recognition by bacterial products. We found that exposure to bacterial endotoxin from 4 to 6 weeks of age did not affect disease progression, whereas an equipotent dose of cytosine-guanine (CpG)-DNA, a synthetic mimic of bacterial DNA, accelerated all aspects of Alport nephropathy and reduced the overall lifespan of Col4a3-deficient mice. This effect was associated with a significant increase of renal CD11b + /Ly6C(hi) macrophages, intrarenal production of inducible nitric oxide synthase, tumor necrosis factor (TNF)-alpha, interleukin-12, and CXCL10, and loss of podocytes. TNF-alpha was essential for acceleration of Alport nephropathy, as etanercept (a soluble TNF-alpha receptor) entirely abrogated the CpG-DNA effect. Thus, systemic exposure to CpG-DNA induces classically activated (M1) macrophages that enhance intrarenal inflammation and disease progression. Hence, factors that modulate the phenotype of renal macrophages can affect the progression of Alport nephropathy and, potentially, other types of chronic kidney diseases. Kidney International (2011) 79, 189-198; doi:10.1038/ki.2010.373; published online 20 October 2010"],["dc.identifier.doi","10.1038/ki.2010.373"],["dc.identifier.isi","000285732900009"],["dc.identifier.pmid","20962742"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24476"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0085-2538"],["dc.title","Bacterial CpG-DNA accelerates Alport glomerulosclerosis by inducing an M1 macrophage phenotype and tumor necrosis factor-alpha-mediated podocyte loss"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","731"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","734"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Borza, Dorin-Bogdan"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.contributor.author","Licht, Christoph"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Segerer, Stephan"],["dc.contributor.author","Torra, Roser"],["dc.contributor.author","Gubler, Marie-Claire"],["dc.contributor.author","Heidet, Laurence"],["dc.contributor.author","Harvey, Scott"],["dc.contributor.author","Cosgrove, Dominic"],["dc.contributor.author","Lees, George"],["dc.contributor.author","Kashtan, Clifford E."],["dc.contributor.author","Gregory, Martin"],["dc.contributor.author","Savige, Judy"],["dc.contributor.author","Ding, Jie"],["dc.contributor.author","Thorner, Paul"],["dc.contributor.author","Abrahamson, Dale R."],["dc.contributor.author","Antignac, Corinne"],["dc.contributor.author","Tryggvason, Karl"],["dc.contributor.author","Hudson, Billy"],["dc.contributor.author","Miner, Jeffrey H."],["dc.date.accessioned","2018-11-07T08:32:22Z"],["dc.date.available","2018-11-07T08:32:22Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1093/ndt/gfn722"],["dc.identifier.isi","000263605000011"],["dc.identifier.pmid","19110486"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17328"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0931-0509"],["dc.title","Stem cell therapy for Alport syndrome: the hope beyond the hype"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","494"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","501"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Licht, Christoph"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.contributor.author","Hoppe, Bernd"],["dc.contributor.author","Beck, Bodo"],["dc.contributor.author","Toenshoff, Burkhard"],["dc.contributor.author","Hoecker, Britta"],["dc.contributor.author","Wygoda, Simone"],["dc.contributor.author","Ehrich, Jochen H. H."],["dc.contributor.author","Pape, Lars"],["dc.contributor.author","Konrad, Martin"],["dc.contributor.author","Rascher, Wolfgang"],["dc.contributor.author","Doetsch, Joerg"],["dc.contributor.author","Mueller-Wiefel, Dirk E."],["dc.contributor.author","Hoyer, Peter F."],["dc.contributor.author","Knebelmann, Bertrand"],["dc.contributor.author","Pirson, Yves"],["dc.contributor.author","Grunfeld, Jean-Pierre"],["dc.contributor.author","Niaudet, Patrick"],["dc.contributor.author","Cochat, Pierre"],["dc.contributor.author","Heidet, Laurence"],["dc.contributor.author","Lebbah, Said"],["dc.contributor.author","Torra, Roser"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Lange, Katharina"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Weber, Manfred"],["dc.date.accessioned","2018-11-07T09:13:13Z"],["dc.date.available","2018-11-07T09:13:13Z"],["dc.date.issued","2012"],["dc.description.abstract","Alport syndrome inevitably leads to end-stage renal disease and there are no therapies known to improve outcome. Here we determined whether angiotensin-converting enzyme inhibitors can delay time to dialysis and improve life expectancy in three generations of Alport families. Patients were categorized by renal function at the initiation of therapy and included 33 with hematuria or microalbuminuria, 115 with proteinuria, 26 with impaired renal function, and 109 untreated relatives. Patients were followed for a period whose mean duration exceeded two decades. Untreated relatives started dialysis at a median age of 22 years. Treatment of those with impaired renal function significantly delayed dialysis to a median age of 25, while treatment of those with proteinuria delayed dialysis to a median age of 40. Significantly, no patient with hematuria or microalbuminuria advanced to renal failure so far. Sibling pairs confirmed these results, showing that earlier therapy in younger patients significantly delayed dialysis by 13 years compared to later or no therapy in older siblings. Therapy significantly improved life expectancy beyond the median age of 55 years of the no-treatment cohort. Thus, Alport syndrome is treatable with angiotensin-converting enzyme inhibition to delay renal failure and therapy improves life expectancy in a time-dependent manner. This supports the need for early diagnosis and early nephroprotective therapy in oligosymptomatic patients. Kidney International (2012) 81, 494-501; doi:10.1038/ki.2011.407; published online 14 December 2011"],["dc.identifier.doi","10.1038/ki.2011.407"],["dc.identifier.isi","000300377000011"],["dc.identifier.pmid","22166847"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27122"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0085-2538"],["dc.title","Early angiotensin-converting enzyme inhibition in Alport syndrome delays renal failure and improves life expectancy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","120"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","131"],["dc.bibliographiccitation.volume","226"],["dc.contributor.author","Ryu, M. I."],["dc.contributor.author","Mulay, Shrikant R."],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.date.accessioned","2018-11-07T09:16:10Z"],["dc.date.available","2018-11-07T09:16:10Z"],["dc.date.issued","2012"],["dc.description.abstract","Chronic renal failure involves the progressive loss of renal parenchymal cells. For example, Alport syndrome develops from mutated type IV collagen that fosters the digestion of glomerular basement membranes and podocyte loss, followed by progressive glomerulosclerosis, ie Alport nephropathy. Here we show that autosomal recessive Alport nephropathy in collagen 4a3-deficient mice is associated with increased intrarenal expression of the pro-apoptotic cytokine tumour necrosis factor-alpha (TNF-alpha) in glomerular cells including podocytes as well as in infiltrating leukocytes. We therefore hypothesized that TNF-alpha contributes to Alport glomerulosclerosis by inducing podocyte apoptosis. To address this issue, we treated 4-week-old collagen 4a3-deficient mice with either vehicle or the TNF-alpha antagonist etanercept for a period of 5 weeks. Etanercept treatment prolonged mean survival from 68 to 81 days as compared to vehicle-treated mice. The beneficial effect of etanercept on survival was associated with a significant improvement of the glomerulosclerosis score, proteinuria, and the glomerular filtration rate at 9 weeks of age. Etanercept treatment specifically reduced the numbers of apoptotic podocytes, increased total podocyte counts, and increased the renal mRNA expression of nephrin and podocin without affecting markers of renal inflammation. TNF-alpha-induced podocyte loss is a previously unrecognized pathological mechanism of Alport glomerulosclerosis, and TNF-alpha blockade might be a therapeutic option to delay the progression of Alport nephropathy and potentially of other forms of glomerulosclerosis. Copyright (C) 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.2979"],["dc.identifier.isi","000298257300012"],["dc.identifier.pmid","21953121"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27870"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0022-3417"],["dc.title","Tumour necrosis factor-alpha drives Alport glomerulosclerosis in mice by promoting podocyte apoptosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","582"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Human Pathology"],["dc.bibliographiccitation.lastpage","593"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Jedlicka, Jan"],["dc.contributor.author","Soleiman, Afschin"],["dc.contributor.author","Draganovici, Dan"],["dc.contributor.author","Mandelbaum, Jana"],["dc.contributor.author","Ziegler, Urs"],["dc.contributor.author","Regele, Heinz"],["dc.contributor.author","Wuethrich, Rudolf P."],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.contributor.author","Segerer, Stephan"],["dc.date.accessioned","2018-11-07T08:44:32Z"],["dc.date.available","2018-11-07T08:44:32Z"],["dc.date.issued","2010"],["dc.description.abstract","The Alport syndrome is a hereditary glomerular disease linked to structural abnormalities of collagen IV. In a mouse model of Alport syndrome, the interstitial lymphocyte influx was important for disease progression. CXCR3 is a chemokine receptor involved in lymphocyte recruitment to the kidney. We hypothesized that CXCR3-positive T cells might be involved in human Alport syndrome. Immunohistochemistry was performed on formalin-fixed, paraffin-embedded biopsies from 17 patients with Alport syndrome, 10 with immunoglobulin A (IgA) nephropathy, and 11 healthy donor kidneys. We investigated the expression of the alpha 5 chain of collagen IV to confirm the morphologic diagnosis, the chemokine receptor CXCR3 and CD3-positive T cells. Alport syndrome biopsies demonstrated a complete loss of the alpha 5 chain of collagen IV from the glomerular basement membrane and the morphologic features consistent with Alport syndrome on electron microscopy. A prominent number of CXCR3-positive cells were found in the tubulointerstitium. Most of the CXCR3-positive cells were CD3-positive T cells, demonstrated by double-labeling in selected biopsies. The number of CXCR3-positive cells in kidneys with Alport syndrome correlated with serum creatinine (P < .05) and with morphologic features of a progressive disease (eg, interstitial fibrosis, glomerulosclerosis, and tubular atrophy). The severity of interstitial CXCR3-positive cell influx was similar in Alport syndrome as compared to immunoglobulin A nephropathy. The noninflammatory glomerular lesion of Alport syndrome is associated with prominent interstitial accumulation of CD3- and CXCR3-positive lymphocytes. The degree of infiltration correlated with renal function. We speculate that targeting T lymphocytes, for example, by CXCR3 blocking agents, might be a novel approach to inhibit disease progression in patients with Alport syndrome. (C) 2010 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.humpath.2009.08.024"],["dc.identifier.isi","000275940000015"],["dc.identifier.pmid","20004949"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20220"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","0046-8177"],["dc.title","Interstitial inflammation in Alport syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]