Job offer

PhD Position in T cell Immunology
PhD Position in T cell Immunology

PhD or Postdoc positions at the HCTI

Collaborate Research Unit, CRU1192/SFB1192 and HCTI (Hamburg Center for Translational Immunology)

The project C3 "High-dimensional single cell profiling in immune-mediated glomerular diseases" of SFB1192 is a joint project of PD Dr. Christian Krebs, Prof. Dr. Ulf Panzer (both Nephrology/Translational Immunology, UKE) and Prof. Stefan Bonn (Institute of Medical Systemsbiology, ZMNH/UKE), which investigates the organ-specific immune response (

The project deals with high-dimensional single cell analysis of immune cells in autoimmune diseases (Krebs et al. Science Immunolgy 2020; Marouf et al. Nature Communications 2020; Zhao et al. Science Immunology 2021). The newly established research profile area HCTI, including a new research building, offers optimal conditions for international top-level research in the field of immunology and systems biology.

The project deals with high-dimensional single cell analysis of immune cells in autoimmune diseases (Krebs et al. Science Immunolgy 2020; Marouf et al. Nature Communications 2020).

Your tasks:

  • Analysis of in-house generated single cell RNA-sequencing data sets
  • Integrative data analysis
  • Cooperation with different projects in the SFB1192
  • Development of new single cell OMICS analysis technologies

Your profile:

  • PhD (or MSc) in bioinformatics, computer science, molecular life sciences, biochemistry, biology or a relevant field
  • Experience with Python, R, Java, SQL and relevant analysis packages
  • Good knowledge of presenting research results
  • Good knowledge of English due to the international orientation of the working groups
  • Prerequisite: Willingness to learn and develop single cell data analysis
  • Ability to work in a team, flexibility

For further information, please contact:

PD Dr. Christian Krebs: (, Twitter: @Krebs_lab)

Prof. Dr. Stefan Bonn:

We would be happy to receive your application by e-mail: or postal: Universitätsklinikum Hamburg-Eppendorf, GB Personal, Recht & Organisation, Recruitment, Martinistr. 52, 20246 Hamburg (reference code 2021-603)

For further information

Heterogeneity and Plasticity of T cells in the Kidney

Plastizität und Stabilität von T-Zellen
Stability and tolerance-induction in renal Th17 cells

Plasticity and stability of Th17 cells in renal autoimmune diseases

T cells play a critical role in the pathogenesis in autoimmune diseases, by their ability to differentiate into pathogenic effector Th1 and Th17 cells or protective regulatory T cells (Treg). This includes human and experimental glomerulonephritis. Classically, these CD4+ T cell subsets have been viewed as terminally differentiated lineages with limited flexibility.

Recent data suggests that CD4+ T cells and Th17 cells in particular have a high degree of plasticity in the brain and intestine, where Th17 can produce IFN-γ and transdifferentiate into Th1 cells. In addition, we found that Th17 cells can also upregulate IL-10 and acquire a regulatory phenotype.

In experimental glomerulonephritis, we found that Th17 cells have very limited spontaneous plasticity in the kidney. However, we were able to promote a regulatory phenotype of Th17 cells in the kidney using CD3-specific antibody treatment. The mechanisms that control stability and transdifferentiation of Th17 cells towards Th1 or regulatory T cells are incompletely understood. In this project we therefore aim to study Th17 cell plasticity in experimental crescentic GN.

Our long-term goal is to identify mechanisms for a shift of Th17 cells towards a regulatory
phenotype that could be used as a therapeutic strategy in GN patients in the future.

Analyse von T-Zellen aus der Niere eines Patienten mit ANCA-assoziierter Glomerulonephritis.
t-SNE of transcritional profiling of T cells

Heterogeneity of T cells in the kidney

CD4+ T cells are key components in the pathogenesis of renal autoimmune diseases. In order to understand the biology of renal T cells we aim to comprehensively characterize these cells by flow cytometry and transcriptional profiling at the single cell level from patients with glomerulonephritis. These studies will pave the way to more specific and less toxic treatment in individual patients.

Renal TRM17 cells
Renal TRM17 cells

Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease

Autoimmunity promoterTissue-resident memory T (TRM) cells are involved in peripheral immunity against reinfection, but their role in autoimmunity is unclear. Krebs et al. examine the contribution of TRM cells in patients with antineutrophil cytoplasmic antibody (ANCA)–dependent glomerulonephritis (GN). They identified multiple T cell subsets in healthy kidney tissue biopsies, but a marked increase in CD4+ TRM cells was seen in kidney biopsies from patients with ANCA-GN. They infected mice with Staphylococcus aureus, which induced renal TH17 cells that had a TRM cell phenotype and persisted in kidney tissue. In a mouse model of crescentic GN, S. aureus infection aggravated kidney pathology and appeared to drive localized renal autoimmune responses. These findings provide critical insight into the role of CD4+ TRM cells in contributing to autoimmune disease.

about the PI

Christian Krebs - Arbeitsgruppenleiter
PD Dr. Christian Krebs

Christian F. Krebs is Privatdozent and principal investigator in the Division of Nephrology, Universitätsklinikum Hamburg-Eppendorf, Germany.

He studied Medicine in Göttingen and Hamburg, and obtained his MD at the Institute of Immunology in Hamburg, Germany. He trained in Internal Medicine and Nephrology at the III, Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Germany and received his habilitation in 2014.

His research interests are T cells in settings of autoimmunity and he has intensively addressed the role of T-helper (TH)17 cells in glomerulonephritis in the past few years. His group is focusing on state-of-the-art characterization and therapeutic targeting of kidney infiltrating T cells.


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Lab members


  • 2021
  • 2020
  • 2019
  • 2018
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  • 2015
  • 2014
  • 2013
  • 2012
  • 2011
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  • 2005
  • 2003

An extracellular vesicle-related gene expression signature identifies high-risk patients in medulloblastoma
Albert T, Interlandi M, Sill M, Graf M, Moreno N, Menck K, Rohlmann A, Melcher V, Korbanka S, Meyer Zu Hörste G, Lautwein T, Frühwald M, Krebs C, Holdhof D, Schoof M, Bleckmann A, Missler M, Dugas M, Schüller U, Jäger N, Pfister S, Kerl K
NEURO-ONCOLOGY. 2021;23(4):586-598.

Tissue-specific therapy in immune-mediated kidney diseases: new ARGuments for targeting the IL-23/IL-17 axis
Krebs C, Turner J, Riedel J, Panzer U
J CLIN INVEST. 2021;131(12):.

Lack of Evidence for an Association between Previous HEV Genotype-3 Exposure and Glomerulonephritis in General
Pischke S, Tamanaei S, Mader M, Wiesch J, Petersen-Benz C, Haddad M, Addo M, Schmidt T, Huber T, Krebs C, Steinmetz O, Turner J, Hoxha E, Horvatits T
PATHOGENS. 2021;11(1):.

Single-cell atlas of hepatic T cells reveals expansion of liver-resident naive-like CD4+ T cells in primary sclerosing cholangitis
Poch T, Krause J, Casar C, Liwinski T, Glau L, Kaufmann M, Ahrenstorf A, Hess L, Ziegler A, Martrus G, Lunemann S, Sebode M, Li J, Schwinge D, Krebs C, Franke A, Friese M, Oldhafer K, Fischer L, Altfeld M, Lohse A, Huber S, Tolosa E, Gagliani N, Schramm C
J HEPATOL. 2021;75(2):414-423.

Kreatininanstieg, Fieber und Hämoptysen: „Double trouble“
Riedel J, Wiech T, Krebs C, Panzer U
Der Nephrologe. 2021 [Epub ahead of print];1-4.

IL-17 receptor c signaling controls CD4+TH17 immune responses and tissue injury in immune-mediated kidney diseases
Schmidt T, Luebbe J, Kilian C, Riedel J, Hiekmann S, Asada N, Ginsberg P, Robben L, Song N, Kaffke A, Peters A, Borchers A, Flavell R, Gagliani N, Pelzcar P, Huber S, Huber T, Turner J, Paust H, Krebs C, Panzer U
J AM SOC NEPHROL. 2021;32(12):3081-3098.

T cell plasticity in renal autoimmune disease
Soukou S, Huber S, Krebs C
CELL TISSUE RES. 2021;385(2):323-333.

Kidney organoid systems for studies of immune-mediated kidney diseases: challenges and opportunities
Stein M, Braun F, Krebs C, Bunders M
CELL TISSUE RES. 2021;385(2):457-473.

A fetal wave of human type 3 effector γδ cells with restricted TCR diversity persists into adulthood
Tan L, Fichtner A, Bruni E, Odak I, Sandrock I, Bubke A, Borchers A, Schultze-Florey C, Koenecke C, Förster R, Jarek M, von Kaisenberg C, Schulz A, Chu X, Zhang B, Li Y, Panzer U, Krebs C, Ravens S, Prinz I
SCI IMMUNOL. 2021;6(58):.

Clonal expansion and activation of tissue-resident memory-like Th17 cells expressing GM-CSF in the lungs of severe COVID-19 patients
Zhao Y, Kilian C, Turner J, Bosurgi L, Roedl K, Bartsch P, Gnirck A, Cortesi F, Schultheiß C, Hellmig M, Enk L, Hausmann F, Borchers A, Wong M, Paust H, Siracusa F, Scheibel N, Herrmann M, Rosati E, Bacher P, Kylies D, Jarczak D, Lütgehetmann M, Pfefferle S, Steurer S, Zur Wiesch J, Puelles V, Sperhake J, Addo M, Lohse A, Binder M, Huber S, Huber T, Kluge S, Bonn S, Panzer U, Gagliani N, Krebs C
SCI IMMUNOL. 2021;6(56):.

Single-cell biology to decode the immune cellular composition of kidney inflammation.
Zhao Y, Panzer U, Bonn S, Krebs C
CELL TISSUE RES. 2021;385(2):435-443.

Deep learning-based molecular morphometrics for kidney biopsies
Zimmermann M, Klaus M, Wong M, Thebille A, Gernhold L, Kuppe C, Halder M, Kranz J, Wanner N, Braun F, Wulf S, Wiech T, Panzer U, Krebs C, Hoxha E, Kramann R, Huber T, Bonn S, Puelles V
JCI INSIGHT. 2021;6(7):e144779.

Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease
Krebs C, Reimers D, Zhao Y, Paust H, Bartsch P, Nuñez S, Rosemblatt M, Hellmig M, Kilian C, Borchers A, Enk L, Zinke M, Becker M, Schmid J, Klinge S, Wong M, Puelles V, Schmidt C, Bertram T, Stumpf N, Hoxha E, Meyer-Schwesinger C, Lindenmeyer M, Cohen C, Rink M, Kurts C, Franzenburg S, Koch-Nolte F, Turner J, Riedel J, Huber S, Gagliani N, Huber T, Wiech T, Rohde H, Bono M, Bonn S, Panzer U, Mittrücker H
SCI IMMUNOL. 2020;5(50):.

Drawing a single-cell landscape of the human kidney in (pseudo)-space and time
Krebs C, Schlitzer A, Kurts C
KIDNEY INT. 2020;97(5):842-844.

Realistic in silico generation and augmentation of single-cell RNA-seq data using generative adversarial networks
Marouf M, Machart P, Bansal V, Kilian C, Magruder D, Krebs C, Bonn S
NAT COMMUN. 2020;11(1):166.

Role of regulatory T cells in experimental autoimmune glomerulonephritis
Klinge S, Yan K, Reimers D, Brede K, Schmid J, Paust H, Krebs C, Panzer U, Hopfer H, Mittrücker H
AM J PHYSIOL-RENAL. 2019;316(3):F572-F581.

Single-Cell Transcriptomics Identifies the Adaptation of Scart1+ Vγ6+ T Cells to Skin Residency as Activated Effector Cells
Tan L, Sandrock I, Odak I, Aizenbud Y, Wilharm A, Barros-Martins J, Tabib Y, Borchers A, Amado T, Gangoda L, Herold M, Schmidt-Supprian M, Kisielow J, Silva-Santos B, Koenecke C, Hovav A, Krebs C, Prinz I, Ravens S
CELL REP. 2019;27(12):3657-3671.e4.

Molecular and functional heterogeneity of IL-10-producing CD4+ T cells
Brockmann L, Soukou S, Steglich B, Czarnewski P, Zhao L, Wende S, Bedke T, Ergen C, Manthey C, Agalioti T, Geffken M, Seiz O, Parigi S, Sorini C, Geginat J, Fujio K, Jacobs T, Roesch T, Izbicki J, Lohse A, Flavell R, Krebs C, Gustafsson J, Antonson P, Roncarolo M, Villablanca E, Gagliani N, Huber S
NAT COMMUN. 2018;9(1):5457.

Plasticity and heterogeneity of Th17 in immune-mediated kidney diseases
Krebs C, Panzer U
J AUTOIMMUN. 2018;87:61-68.

IL-17C/IL-17 Receptor E Signaling in CD4 T Cells Promotes T17 Cell-Driven Glomerular Inflammation
Krohn S, Nies J, Kapffer S, Schmidt T, Riedel J, Kaffke A, Peters A, Steinmetz O, Krebs C, Turner J, Brix S, Paust H, Stahl R, Panzer U
J AM SOC NEPHROL. 2018;29(4):1210-1222.

Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3 Regulatory T Cells
Mathies F, Steffens N, Kleinschmidt D, Stuhlmann F, Huber F, Roy U, Meyer T, Luetgehetmann M, von Petersdorff M, Seiz O, Herkel J, Schramm C, Flavell R, Gagliani N, Krebs C, Panzer U, Abdullah Z, Strowig T, Bedke T, Huber S
J IMMUNOL. 2018;201(12):3558-3568.

IL-10 Receptor Signaling Is Essential for TR1 Cell Function In Vivo
Brockmann L, Gagliani N, Steglich B, Giannou A, Kempski J, Pelczar P, Geffken M, Mfarrej B, Huber F, Herkel J, Wan Y, Esplugues E, Battaglia M, Krebs C, Flavell R, Huber S
J IMMUNOL. 2017;198(3):1130-1141.

T helper type 17 cells in immune-mediated glomerular disease
Krebs C, Schmidt T, Riedel J, Panzer U
NAT REV NEPHROL. 2017;13(10):647-659.

ISN Nexus 2016 Symposia: Translational Immunology in Kidney Disease—The Berlin Roadmap
Anders H, Rovin B, Jayne D, Brunetta P, Coppo R, Davidson A, Devarapu S, de Zeeuw D, Duffield J, Eulberg D, Fierro A, Floege J, Frese S, Guillevin L, Holdsworth S, Hughes J, Kettritz R, Kluger M, Krebs C, Lapteva L, Levin A, Li J, Lightstone L, Mack M, Mansouri L, McAdoo S, McKinney E, Panzer U, Parikh S, Pusey C, Putterman C, Rabelink T, Radbruch A, Rees A, Reilly M, Reinders M, Remuzzi G, Ruggenenti P, Sacks S, Schall T, Meyer-Schwesinger C, Sharma K, Suzuki Y, Tomas N, Zhao M
KIDNEY INT REP. 2016;1(4):327-339.

Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney
Krebs C, Paust H, Krohn S, Koyro T, Brix S, Riedel J, Bartsch P, Wiech T, Meyer-Schwesinger C, Huang J, Fischer N, Busch C, Mittrücker H, Steinhoff U, Stockinger B, Perez L, Wenzel U, Janneck M, Steinmetz O, Gagliani N, Stahl R, Huber S, Turner J, Panzer U
IMMUNITY. 2016;45(5):1078-1092.

CD4+ T Cell Fate in Glomerulonephritis: A Tale of Th1, Th17, and Novel Treg Subtypes
Krebs C, Steinmetz O
MEDIAT INFLAMM. 2016;2016:.

Plasticity of Th17 Cells in Autoimmune Kidney Diseases
Krebs C, Turner J, Paust H, Kapffer S, Koyro T, Krohn S, Ufer F, Friese M, Flavell R, Stockinger B, Steinmetz O, Stahl R, Huber S, Panzer U
J IMMUNOL. 2016;197(2):449-57.

CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN
Paust H, Riedel J, Krebs C, Turner J, Brix S, Krohn S, Velden J, Wiech T, Kaffke A, Peters A, Bennstein S, Kapffer S, Meyer-Schwesinger C, Wegscheid C, Tiegs G, Thaiss F, Mittrücker H, Steinmetz O, Stahl R, Panzer U
J AM SOC NEPHROL. 2016;27(7):1933-42.

IL-17F Promotes Tissue Injury in Autoimmune Kidney Diseases
Riedel J, Paust H, Krohn S, Turner J, Kluger M, Steinmetz O, Krebs C, Stahl R, Panzer U
J AM SOC NEPHROL. 2016;27(12):3666-3677.

Immune Mechanisms in Arterial Hypertension
Wenzel U, Turner J, Krebs C, Kurts C, Harrison D, Ehmke H
J AM SOC NEPHROL. 2016;27(3):677-86.

CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN
Brix S, Stege G, Disteldorf E, Hoxha E, Krebs C, Krohn S, Otto B, Klätschke K, Herden E, Heymann F, Lira S, Tacke F, Wolf G, Busch M, Jabs W, Özcan F, Keller F, Beige J, Wagner K, Helmchen U, Noriega M, Wiech T, Panzer U, Stahl R
J AM SOC NEPHROL. 2015;26(9):2105-2117.

CXCL5 drives neutrophil recruitment in TH17-mediated GN
Disteldorf E, Krebs C, Paust H, Turner J, Nouailles G, Tittel A, Meyer-Schwesinger C, Stege G, Brix S, Velden J, Wiech T, Helmchen U, Steinmetz O, Peters A, Bennstein S, Kaffke A, Llanto C, Lira S, Mittrücker H, Stahl R, Kurts C, Kaufmann S, Panzer U
J AM SOC NEPHROL. 2015;26(1):55-66.

Function of the Th17/interleukin-17A immune response in murine lupus nephritis
Schmidt T, Paust H, Krebs C, Turner J, Kaffke A, Bennstein S, Koyro T, Peters A, Velden J, Hünemörder S, Haag F, Steinmetz O, Mittrücker H, Stahl R, Panzer U
ARTHRITIS RHEUMATOL. 2015;67(2):475-87.

Deficiency of the interleukin 17/23 axis accelerates renal injury in mice with deoxycorticosterone acetate+angiotensin ii-induced hypertension
Krebs C, Lange S, Niemann G, Rosendahl A, Lehners A, Meyer-Schwesinger C, Stahl R, Benndorf R, Velden J, Paust H, Panzer U, Ehmke H, Wenzel U
HYPERTENSION. 2014;63(3):565-71.

Increased expression of (pro)renin receptor does not cause hypertension or cardiac and renal fibrosis in mice
Rosendahl A, Niemann G, Lange S, Ahadzadeh E, Krebs C, Contrepas A, van Goor H, Wiech T, Bader M, Schwake M, Peters J, Stahl R, Nguyen G, Wenzel U
LAB INVEST. 2014;94(8):863-72.

MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN
Krebs C, Kapffer S, Paust H, Schmidt T, Bennstein S, Peters A, Stege G, Brix S, Meyer-Schwesinger C, Müller R, Turner J, Steinmetz O, Wolf G, Stahl R, Panzer U
J AM SOC NEPHROL. 2013;24(12):1955-65.

AT1 antagonism and renin inhibition in mice: pivotal role of targeting angiotensin II in chronic kidney disease.
Fraune C, Lange S, Krebs C, Hölzel A, Baucke J, Divac N, Schwedhelm E, Streichert T, Velden J, Garrelds I, Danser A, Frenay A, van Goor H, Jankowski V, Stahl R, Nguyen G, Wenzel U
AM J PHYSIOL-RENAL. 2012;303(7):1037-1048.

CCR5 deficiency does not reduce hypertensive end-organ damage in mice.
Krebs C, Fraune C, Schmidt-Haupt R, Turner J, Panzer U, Quang M, Tannapfel A, Velden J, Stahl R, Wenzel U
AM J HYPERTENS. 2012;25(4):479-486.

Glomerulonephritiden – Genetische Aspekte
Krebs C, Panzer U
Dialyse aktuell. 2012;16(9):523-527.

Chemokines play a critical role in the cross-regulation of Th1 and Th17 immune responses in murine crescentic glomerulonephritis.
Paust H, Turner J, Riedel J, Disteldorf E, Peters A, Schmidt T, Krebs C, Velden J, Mittrücker H, Steinmetz O, Stahl R, Panzer U
KIDNEY INT. 2012;82(1):72-83.

Immature renal dendritic cells recruit regulatory CXCR6(+) invariant natural killer T cells to attenuate crescentic GN.
Riedel J, Paust H, Turner J, Tittel A, Krebs C, Disteldorf E, Wegscheid C, Tiegs G, Velden J, Mittrücker H, Garbi N, Stahl R, Steinmetz O, Kurts C, Panzer U
J AM SOC NEPHROL. 2012;23(12):1987-2000.

Dimethylarginine dimethylaminohydrolase1 is an organ-specific mediator of end organ damage in a murine model of hypertension.
Sydow K, Schmitz C, von Leitner E, von Leitner R, Klinke A, Atzler D, Krebs C, Wieboldt H, Ehmke H, Schwedhelm E, Meinertz T, Blankenberg S, Böger R, Magnus T, Baldus S, Wenzel U
PLOS ONE. 2012;7(10):48150.

IL-17A production by renal γδ T cells promotes kidney injury in crescentic GN.
Turner J, Krebs C, Tittel A, Paust H, Meyer-Schwesinger C, Bennstein S, Steinmetz O, Prinz I, Magnus T, Korn T, Stahl R, Kurts C, Panzer U
J AM SOC NEPHROL. 2012;23(9):1486-1495.

Protective role for CCR5 in murine lupus nephritis.
Turner J, Paust H, Mathey S, Bramke P, Krebs C, Steinmetz O, Velden J, Haag F, Stahl R, Panzer U
AM J PHYSIOL-RENAL. 2012;302(11):1503-1515.

Podocytes of AT2 receptor knockout mice are protected from angiotensin II-mediated RAGE induction.
Rüster C, Franke S, Wenzel U, Schmidt-Haupt R, Fraune C, Krebs C, Wolf G
AM J NEPHROL. 2011;34(4):309-317.

Characterisation of a novel glycosylphosphatidylinositol-anchored mono-ADP-ribosyltransferase isoform in ovary cells.
Stilla A, Simone D, Dani N, Krebs C, Arrizza A, Corda D, Haag F, Koch Nolte F, Maria D
EUR J CELL BIOL. 2011;90(8):665-677.

The angiotensin II type 2 receptor in renal disease.
Wenzel U, Krebs C, Benndorf R
J RENIN-ANGIO-ALDO S. 2010;11(1):37-41.

Angiotensin II type 2 receptor deficiency aggravates renal injury and reduces survival in chronic kidney disease in mice.
Benndorf R, Krebs C, Hirsch-Hoffmann B, Schwedhelm E, Cieslar G, Schmidt-Haupt R, Steinmetz O, Meyer-Schwesinger C, Thaiss F, Haddad M, Fehr S, Heilmann A, Helmchen U, Hein L, Ehmke H, Stahl R, Böger R, Wenzel U
KIDNEY INT. 2009;75(10):1039-1049.

NAD+ and ATP released from injured cells induce P2X7-dependent shedding of CD62L and externalization of phosphatidylserine by murine T cells.
Scheuplein F, Schwarz N, Adriouch S, Krebs C, Bannas P, Rissiek B, Seman M, Haag F, Koch Nolte F
J IMMUNOL. 2009;182(5):2898-2908.

Rapid development of severe end-organ damage in C57BL/6 mice by combining DOCA salt and angiotensin II.
Kirchhoff F, Krebs C, Abdulhag U, Meyer-Schwesinger C, Maas R, Helmchen U, Hilgers K, Wolf G, Stahl R, Wenzel U
KIDNEY INT. 2008;73(5):643-650.

Effect of (pro)renin receptor inhibition by a decoy peptide on renal damage in the clipped kidney of Goldblatt rats.
Krebs C, Weber M, Steinmetz O, Meyer-Schwesinger C, Stahl R, Danser A, Garrelds I, van Goor H, Nguyen G, Müller D, Wenzel U
KIDNEY INT. 2008;74(6):823-824.

[Quality of life under antihypertensive therapy: essentially for compliance]
Wenzel U, Krebs C
MMW Fortschr Med. 2008;150(24):30-32.

Antihypertensive therapy upregulates renin and (pro)renin receptor in the clipped kidney of Goldblatt hypertensive rats.
Krebs C, Hamming I, Sadaghiani S, Steinmetz O, Meyer-Schwesinger C, Fehr S, Stahl R, Garrelds I, Danser A, van Goor H, Contrepas A, Nguyen G, Wenzel U
KIDNEY INT. 2007;72(6):725-730.

Antihypertensive therapy induces compartment-specific chemokine expression and a Th1 immune response in the clipped kidney of Goldblatt hypertensive rats.
Steinmetz O, Sadaghiani S, Panzer U, Krebs C, Meyer-Schwesinger C, Streichert T, Fehr S, Hamming I, van Goor H, Stahl R, Wenzel U
AM J PHYSIOL-RENAL. 2007;292(2):876-887.

Management of arterial hypertension in obese patients.
Wenzel U, Krebs C
CURR HYPERTENS REP. 2007;9(6):491-497.

ADP-ribosylation of membrane proteins: unveiling the secrets of a crucial regulatory mechanism in mammalian cells.
Koch-Nolte F, Adriouch S, Bannas P, Krebs C, Scheuplein F, Seman M, Haag F
ANN MED. 2006;38(3):188-199.

CD38 controls ADP-ribosyltransferase-2-catalyzed ADP-ribosylation of T cell surface proteins
Krebs C, Adriouch S, Braasch F, Koestner W, Leiter E, Seman M, Lund F, Oppenheimer N, Haag F, Koch-Nolte F
J IMMUNOL. 2005;174(6):3298-305.

Flow cytometric and immunoblot assays for cell surface ADP-ribosylation using a monoclonal antibody specific for ethenoadenosine
Krebs C, Koestner W, Nissen M, Welge V, Parusel I, Malavasi F, Leiter E, Santella R, Haag F, Koch-Nolte F
ANAL BIOCHEM. 2003;314(1):108-15.

NAD-induced T cell death: ADP-ribosylation of cell surface proteins by ART2 activates the cytolytic P2X7 purinoceptor
Seman M, Adriouch S, Scheuplein F, Krebs C, Freese D, Glowacki G, Deterre P, Haag F, Koch-Nolte F
IMMUNITY. 2003;19(4):571-82.

Letzte Aktualisierung aus dem FIS: 16.05.2022 - 03:16 Uhr