CXCL5 Drives Neutrophil Recruitment in TH17-Mediated GN

Disteldorf, Erik; Krebs, Christian; Paust, Hans‐Joachim; Turner, Jan-Eric; Nouailles, Geraldine; Tittel, André P.; Meyer-Schwesinger, Catherine; Stege, Gesa; Brix, Silke R.; Velden, Joachim; Wiech, Thorsten; Helmchen, Udo; Steinmetz, Oliver M.; Peters, Anett; Bennstein, Sabrina Bianca; Kaffke, Anna; Llanto, Chrystel; Lira, Sérgio A.; Mittrücker, Hans‐Willi; Stahl, Rolf A.K.; Kurts, Christian; Kaufmann, Stefan H. E.; Panzer, Ulf

doi:10.1681/asn.2013101061

Cited by 112 publications

(90 citation statements)

References 50 publications

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“…40 per kidney were counted in a blinded manner. All slides were evaluated by Axioskop Light Microscopy (Carl Zeiss, Jena, Germany) and photographed with an Axiocam HRc (Carl Zeiss) or by confocal microscopy with an LSM 510 Metamicroscope using the LSM software.…”

Section: Morphologic Analysesmentioning

confidence: 99%

“…40 Single-cell suspensions were obtained from human biopsies by enzymatic digestion in RPMI1640 with collagenase D (0.4 mg/ml) and deoxyribonuclease type I (10 mg/ml; Roche Diagnostics) at 37°C followed by dissociation with gentle-MACS (Miltenyi Biotec). Samples were filtered through a 30-mm filter before antibody staining and flow cytometry.…”

Section: Analyses In Patients With Anca Gnmentioning

confidence: 99%

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CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN

Paust¹,

Riedel²,

Krebs³

et al. 2015

JASN

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Chemokines and chemokine receptors are implicated in regulatory T cell (Treg) trafficking to sites of inflammation and suppression of excessive immune responses in inflammatory and autoimmune diseases; however, the specific requirements for Treg migration into the inflamed organs and the positioning of these cells within the tissue are incompletely understood. Here, we report that Tregs expressing the T H 1-associated chemokine receptor CXCR3 are enriched in the kidneys of patients with ANCA-associated crescentic GN and colocalize with CXCR3 + effector T cells.

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Section: Morphologic Analysesmentioning

confidence: 99%

Section: Analyses In Patients With Anca Gnmentioning

confidence: 99%

CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN

Paust¹,

Riedel²,

Krebs³

et al. 2015

JASN

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“…As a measure for tubulointerstitial injury, the interstitial area was estimated by point counting of four independent areas of renal cortex per mouse under low magnification (3200) as previously described. 52 …”

Section: Murine Morphologic Analysesmentioning

confidence: 99%

CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN

Brix¹,

Stege²,

Disteldorf³

et al. 2015

Journal of the American Society of Nephrology

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ANCA-associated vasculitis is the most frequent cause of crescentic GN. To define new molecular and/or cellular biomarkers of this disease in the kidney, we performed microarray analyses of renal biopsy samples from patients with ANCA-associated crescentic GN. Expression profiles were correlated with clinical data in a prospective study of patients with renal ANCA disease. CC chemokine ligand 18 (CCL18), acting through CC chemokine receptor 8 (CCR8) on mononuclear cells, was identified as the most upregulated chemotactic cytokine in patients with newly diagnosed ANCA-associated crescentic GN. Macrophages and myeloid dendritic cells in the kidney were detected as CCL18-producing cells. The density of CCL18 + cells correlated with crescent formation, interstitial inflammation, and impairment of renal function. CCL18 protein levels were higher in sera of patients with renal ANCA disease compared with those in sera of patients with other forms of crescentic GN. CCL18 serum levels were higher in patients who suffered from ANCA-associated renal relapses compared with those in patients who remained in remission. Using a murine model of crescentic GN, we explored the effects of the CCL18 murine functional analog CCL8 and its receptor CCR8 on kidney function and morphology. Compared with wild-type mice, Ccr8 2/2 mice had significantly less infiltration of pathogenic mononuclear phagocytes. Furthermore, Ccr8 2/2 mice maintained renal function better and had reduced renal tissue injury. In summary, our data indicate that CCL18 drives renal inflammation through CCR8-expressing cells and could serve as a biomarker for disease activity and renal relapse in ANCA-associated crescentic GN.

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“…Given it capacity of recruiting polymorphonucleated leukocytes, It is hypothesized that the ideal host protective defense against Klebsiella pneumoniae infection is based on the production of memory Th17 cells (Disteldorf et al, 2015). We did not assess the differentiation of naïve lymphocytes in Th17 cells.…”

Section: Resultsmentioning

confidence: 99%