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Institute of Experimental Immunology

1. Research overview
2. Research topics
3. Group members
4. Grant support
5. Principal investigator
6. Publications
 

Research overview

Our common interests are the mechanisms governing antigen-presentation and the ensuing immune response in the defense against infections and in immune-mediated disease. We focus at 3 major topics:
1.) Mechanisms of antigen cross-presentation to cytotoxic CD8 T cells
2.) Peripheral immune tolerance of T and B lymphocytes against self antigens
3.) Role of dendritic cells in diseases, especially in the kidney disease

T lymphocytes (=T cells) defend our body against infections with microbes. They require activation by antigen-presenting cells, in particular dendritic cells (DCs). These DCs collect antigens in various tissues, migrate to draining lymph nodes, and activate the T cells there. The mechanism of cross-presentation enables DCs to activate the CD8+ cytotoxic T cells, which are crucial for the immune defense against viruses, some intracellular bacteriae and tumors (Figure on the right).

We have previously shown that DCs can destroy harmful cytotoxic T cells, and thereby prevent them from damaging our own body. In case of failure of this form of peripheral immune tolerance, which is also known as cross-tolerance, autoimmune diseases arise, such as type I diabetes mellitus or multiple sclerosis (Figure on the left shows common autoimmune diseases). Other forms of peripheral immune tolerance include the induction of regulatory T cells, which can suppress harmful T cells. We are interested in suppression of harmful B cells, and prevention of autoantibody formation, which play important roles in various autoimmune diseases such as glomerulonephritis or rheumatoid arthritis.

 

Our third topic of interest is the role of dendritic cells and other myeloid cells in local immune responses in non-lymphoid tissues, with a special emphasis on the kidney dendritic cells. Here we wish to understand the immune mechanisms underlying diseases such responses as glomerulonephritis and cystitis/pyelonephritis. Furthermore, we study DC's in the eye, the intestine and the heart.

 

 

Research topics
 

Role of Chemokines in Cross-presentation

Verena Semmling, Katharina Hochheiser, Christoph Thaiss; Previous: V. Lukacs-Kornek

Chemokines regulate migration and encounters of immune cells. In cross-presentation, various rare immune cells have to meet. Using various knockout mice we study which chemokine receptors are instrumental in orchestrating their migratory behavior in vivo.
 

Cell-biology of Cross-presentation

Lars Franken, Catherine Gottschalk, previous: S. Burgdorf, Achmet Imam-Chasan, M. Weimershaus, V. Böhnert

Together with Dr. Sven Burgdorf's group (now PI at the LIMES institute of Bonn), we investigate the cell biological mechanisms underlying cross-presentation. We have recently demonstrated that antigens intended for presentation on MHC I or MHC II molecules are internalized by distinct endocytosis mechanisms and targeted into different organelles. Whilst pinocytosis and scavenger receptor-mediated endocytosis introduce antigens into lysosomes for presentation exclusively on MHC II molecules, the mannose receptor routed the antigen into early endosomes, from which it was processed only for presentation on MHC I. After internalization, mannose-receptor-endocytosed antigens were transported out of the endosomes into the cytoplasm for degradation. The resulting peptides were transported back into the same endosomes by TAP, a molecule from the ER, which is recruited to endosomes in a TLR4- and MyD88-dependent fashion. In these endosomes, the antigenic peptides were subsequently loaded on MHC I molecules and transported to the cell membrane for presentation to T cells. Current projects mainly focus on the characterization of the endosomes dedicated to cross-presentation, the export of antigens into the cytoplasm and the influence of antigen modifications and cell type on antigen presentation.
 

Peripheral B cell tolerance

Isis Ludwig-Protugall, Catherine Gottschalk, Janine Gotot, Sonny Leopold, Vera Damuzzo

We are interested in mechanisms of peripheral B cell tolerance against non-lymphatic tissue autoantigens and prevention of autoantibody generation. To study this question, we have generated novel transgenic mice, which allow tracking the response and fate of autoreactive B cells in vivo. Our findings demonstrate that regulatory T cells control autoreactive B cells by blocking their response to autoantigen and by inducing their apoptosis in the autoantigen-draining lymph node and in the spleen.
 

Immune reactions in urinary tract infections

Daniel R. Engel, André Tittel, Marzena Schiwon, Sebastian Gutweiler, Chrystel Llanto, Christina Ohliger; Previous: C. Weisheit

Urinary tract infections are among the most common infections, and are usually due to uropathogenic E. coli bacteriae (UPEC) ascending entering the urethra. UPEC can enter uroepithelial cells, to hide there from immune survey and to reemerge in situations of reduced immune defense. We have developed an animal model that allows studying the underlying immune mechanisms and the consequences for kidney function in detail.
 

 

Role of dendritic cells in immune regulation in non-lymphatic tissues

 André Tittel, Daniel R. Engel, Arne Koscielny, Thorsten Urcyniczok, Anne F. Alex, Juliane Maurer, Simon Teteris; Previous: V. Lukacs-Kornek, E. Hamilton-Williams, F. Heymann, J. Scholz 

1a.    In the healthy kidney:

The kidney constitutively filtrates and concentrates protein below albumin molecular weight. Enriched filtrated antigen is transported cell-independently within two minutes to renal lymph nodes, where they are taken up by resident dendritic cells by mannose-receptor-mediated endocytosis. Such DCs then tolerized specific CD8+ T cells by inducing apoptosis. These findings identify a constitutively active T cell cross-tolerance mechanism, which is independent of steady-state DC migration. It may contribute to preventing unwanted immunity against innocuous circulating proteins.

1b.    In glomerulonephritis:

Glomerulonephritis (GN) is one of the major causes for terminal kidney failure and the need to undergo hemodialysis. Our particular focus is the immunobiology of renal dendritic cells (DC), which form a constitutive tubulointerstitial network, whose function remains to be clarified. We have recently shown that these cells possess a protective role in nephrotoxic nephritis, a model of human rapid progressive crescentic GN. We are interested in the precise underlying mechanisms, including those recruiting DCs into inflamed kidney tissue, the ensuing immune response and in consequences for kidney function and fibrosis. To this end, we employ novel transgenic models that allow dissecting immunity directed against kidney tissue.

1c.    In pyelonephritis:

Little is known about the role of DCs in pyelonephritis, which is also a frequent cause for terminal kidney failure and the need to undergo hemodialysis. We have established a murine model to explore the underlying reasons.

2.    In the intestine:

Intestinal manipulation during abdominal surgery frequently leads to postoperative ileus, causing prolonged morbidity. The clinically leading problem is that the entire intestinal tract, and not only the surgically manipulated areas become paralyzed. We are studying the role of intestinal DCs and T cells in initiating inflammatory processes that paralyze intestinal myocytes in a collaboration with Prof. Dr. Jörg Kalff from the Department of Surgery, University of Bonn University of Bonn Medical Center (KFO115).

3.    In the eye:

Age-dependent macula degeneration is the most prevalent cause of blindness in old age. It is believed to result from persisting inflammatory processes at the retina/choroid, and a role of DCs has been proposed. We are aiming at identifying the exact nature of this role, and explore opportunities for therapeutical interventions in a collabopration with Prof. Dr. Nicole Eter from the Lab of cellular physiology at the Dept. of Ophthalmology of the University of Bonn Medical Center.

4.    In the heart:

In sepsis, the heart function drastically declines, and increases the risk of complications in intensive care patients. We are exploring the role of heart-resident DCs in this condition in a collaboration with PD Dr. Georg Baumgarten from the Department for Anesthesiology, University clinic of Bonn University.

 

Group Members

From left to right:  Janine Gotot, Lars Franken, Catherine Gottschalk, Torsten Urcyniczok, Anne Alex, Katharina Hochheiser, Chrystel Llanto, Lucie Delforge, Christoph Heuser, Isis Ludwig-Portugall, Christian Kurts, Verena Semmling, Vera Damuzzo, Christina Ohliger, Simon Teteris, Marzena Schiwon, Maike Weidgang, André Tittel, Sonny Leopold, Daniel Engel, Martin Otte, Sarah Koudaimi

Not in picture:  Sebastian Gutweiler, Juliane Maurer, Christoph Thaiss

 

Grant support

  • German Research Foundation (Deutsche Forschungsgemeinschaft, DFG)

  • Sonderforschungsbereich 704

  • Sonderforschungsbereich 645

  • Sonderforschungsbereich TR57

  • KFO 115

  • KFO 228

  • EU FP7 project INTRICATE

  • DAAD Go8 student exchange with Australia

  • German National Academic Foundation (Studienstiftung des Deutschen Volkes)

  • Bonfor

 

Principal Investigator

Institutes of Molecular Medicine and Experimental Immunology (IMMEI)

University Clinic of Bonn
Sigmund-Freud-Str. 25
D-53105 Bonn, Germany

Tel: +49-(0) 228-287 11050
Fax: +49-(0) 228-287 11052
ckurts{at}uni-bonn.de

 

1985-91       Studies in physics and medicine, University of Göttingen Germany
1986-91       Fellowship German National Academic Foundation
11/1991       Doctoral thesis at the Department of Immunology (Prof. Dr. O. Götze), University of Göttingen
11/91-4/95   Medical Officer and Research Fellow, Department of Nephrology (Prof. Dr. KM Koch), University of Hannover, Germany
4/95-3/98     Postdoctoral Research Fellow, Thymus Biology Unit (Prof. J. Miller) and Immunology Division (Dr. W.R. Heath),
                   The Walter and Eliza Hall Institute for Medical Research (WEHI), Melbourne Australia
4/98-8/00     Medical Officer and Research Fellow, Department of Nephrology, Hannover
6/1999         Lectureship (Habilitation) for Experimental Nephrology
12/1999       Sir Hans Krebs award for basic medical research
8/2000         Board Certification in general internal medicine (Facharzt)
9/2000         Heisenberg-Fellowship of the deutsche Forschungsgemeinschaft
9/00-3/03     Research Group leader, Dpt. of Nephrology and Clinical Immunology (Prof. Dr. J Floege), University of Aachen
10/02-12/02 Visiting scientist, Steven Schoenberger Group, La Jolla Institute for Allergy and Immunology, San Diego USA
04/2003       Full Professor of Molecular Immunology, Institute for Molecular Medicine and Experimental Immunology, University of Bonn
4/2005         Student Mentor and member of the selection board of the German National Academic Foundation (Studienstiftung des Deutschen Volkes)
10/2005       Board Certification for Clinical Nephrology (Innere Medizin Teilgebiet Nephrologie)
04/2009       Director Institute of Experimental Immunology, University of Bonn
06/2010       Hans-U.-Zollinger Award of the German Society for Nephrology

 

Selected Publications

  1. Kurts, C, Robinson BWS, Knolle PA. 2010. Cross-priming in Health and Disease. Nature Rev Immunol, 10(6): 403-414

  2. Semmling V, Lukacs-Kornek V, Thaiss CA, Quast T, Hochheiser K, Panzer U, Rossjohn J, Perlmutter P, Cao J, Godfrey DI, Savage PB, Knolle PA, Kolanus W, Förster I, Kurts C. Alternative cross-priming through CCL17-CCR4-mediated attraction of CTLs toward NKT cell-licensed DCs. Nature Immunol. 2010 Apr;11(4):313-20. Epub 2010 Feb 28.
    Press release: http://http://www.kompetenznetze.de/service/nachrichten/2010/six-eye-principle-protects-the-body-from-autoimmune-diseases

  3. Semmling V, Thaiss CA, Lukacs-Kornek V, Förster I, Knolle PA, Kurts C. 2010. Quantifying in vivo recruitment of naïve CTL towards individual dendritic cells by standard immunofluorescence histology. Nature Protoc; Epub 2010 Mar 5; 10.1038/nprot.2010.52

  4. Burgdorf S, Schuette V, Semmling V, Hochheiser K, Lukacs-Kornek V, Knolle PA, Kurts C. Steady-state cross-presentation of OVA is mannose receptor-dependent but inhibitable by collagen fragments. Proc Natl Acad Sci USA. 2010 Mar 30;107(13):E48-9

  5. Schurich A, Berg M, Stabenow D, Böttcher J, Kern M, Schild HJ, Kurts C, Schuette V, Burgdorf S, Diehl L, Limmer A, Knolle PA. Dynamic regulation of CD8 T cell tolerance induction by liver sinusoidal endothelial cells. J Immunol. 2010 Apr 15;184(8):4107-14. Epub 2010 Mar 8.

  6. Ilchmann A, Burgdorf S, Scheurer S, Waibler Z, Nagai R, Wellner A, Yamamoto Y, Yamamoto H, Henle T, Kurts C, Kalinke U, Vieths S, Toda M. Glycation of a food allergen by the Maillard reaction enhances its T-cell immunogenicity: role of macrophage scavenger receptor class A type I and II. J Allergy Clin Immunol. 2010 Jan;125(1):175-83.e1-11. Epub 2009 Oct 27.

  7. Heymann F, Meyer-Schwesinger C, Hamilton-Williams EE, Hammerich L, Panzer U, Kaden S, Floege J, Gröne HJ, Kurts C. 2009. Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury. J Clin Invest, 119:1286-97; Epub April 20, 2009 
    Press release: http://bonner-presseblog.de/2009/04/20/bonn-wenn-das-immunsystem-die-eigenen-nieren-bekämpft/

  8. Lutz M, Kurts C. 2009. Induction of peripheral CD4+ T cell tolerance and CD8+ T cell cross-tolerance by conventional dendritic cells. Eur J Immunol, 21;39:2325-2330

  9. Panzer U, Kurts C. 2009. T cell cross-talk with kidney dendritic cells in glomerulonephritis. J Mol Med, Epub Oct 2, DOI 10.1007/s00109-009-0541-5

  10. Paust HJ, Turner JE, Steinmetz OM, Peters A, Heymann F, Hölscher C, Wolf G, Kurts C, Mittrücker HW, Stahl RA, Panzer U. The IL-23/Th17 axis contributes to renal injury in experimental glomerulonephritis. J Am Soc Nephrol. 2009 May;20(5):969-79. Epub 2009 Apr 1.

  11. Schurich A, Böttcher JP, Burgdorf S, Penzler P, Hegenbarth S, Kern M, Dolf A, Endl E, Schultze J, Wiertz E, Stabenow D, Kurts C, Knolle P. 2009. Distinct kinetics and dynamics of cross-presentation in liver sinusoidal endothelial cells compared to dendritic cells. Hepatology, 11:909-919

  12. Klotz L, Hucke S, Thimm D, Classen S, Gaarz A, Schultze J, Edenhofer F, Kurts C, Klockgether T, Limmer A, Knolle P, Burgdorf S. 2009. Increased antigen cross-presentation but impaired cross-priming after activation of PPARg is mediated by up-regulation of B7H1. J Immunol, 183:129-36

  13. Klotz L, Burgdorf S, Dani I, Saijo K, Alferink J, Langhans B, Klockgether T, Frommer F, Cherrier M,. Waisman A, Glass C, Eberl G, Kurts C, Knolle, P. 2009. The nuclear receptor PPAR? controls Th17 differentiation and suppresses Th17 dependent autoimmunity. J Exp Med, 206(10):2079-89

  14. Ludwig-Portugall I, Hamilton-Williams EE, Gotot J, Kurts C. 2009. CD25+ regulatory T cells specifically suppress auto-antibody generation against pancreatic tissue autoantigens. Eur J Immunol, 2009 7:39:225-233

  15. Parish I, Waithman J, Davey GM, Belz GT, Mintern JD, Kurts C, Sutherland RM, Carbone FR, Heath WR. 2009. Tissue destruction caused by cytotoxic T lymphocytes induces deletional tolerance. Proc Natl Acad Sci USA, 106:3901-6

  16. Scholz J, Lukacs-Kornek V, Engel DR, Specht S, Kiss E, Eitner F, Floege J, Groene HJ, Kurts C. 2008. Kidney dendritic cells stimulate IL-10 production in nephrotoxic nephritis and attenuate disease, J Am Soc Nephrol, 19(3): 527-37

  17. Ludwig-Portugall I, Hamilton-Williams EE, Gottschalk C, Kurts C. 2008. Cutting Edge: CD25+ regulatory T cells prevent expansion and induce apoptosis of B cells specific for tissue autoantigens. J Immunol, 181: 4447-

  18. Turner JE, Paust HJ, Steinmetz OM, Peters A, Meyer-Schwesinger C, Heymann F, Helmchen U, Fehr S, Horuk, R, Wenzel U, Kurts C, Mittrücker HW, Stahl RAK, Panzer U 2008. CCR5 deficiency aggravates crescentic glomerulonephritis in mice. J Immunol 181: 6546-56

  19. Engel DR, Maurer J, Tittel A, Weisheit C, Cavlar T, Schumak B, Limmer A, van Rooijen N, Trautwein C, Tacke F, Kurts C. 2008. CCR2 mediates homeostatic and inflammatory release of Gr1HI monocytes from the bone-marrow, but is dispensable for bladder infiltration in bacterial urinary tract infection. J Immunol, 181: 5579-86

  20. Ney JT, Schmidt T, Kurts C, Zhou Q, Eckert D, Felsher D, Schorle H, Knolle P, Tüting T, Barchet W, Büttner R, Limmer A, Gütgemann I. 2009. Autochthonous liver tumors induce systemic T cell tolerance associated with T cell receptor downmodulation. Hepatology, 49:471-81

  21. Burgdorf S, Kurts C. 2008. Endocytosis mechanisms and the cell biology of antigen-presentation. Curr Opin Immunol, 20: 89-95

  22. Burgdorf S, Schölz C, Kautz A, Tampé R, Kurts C. 2008. Spatial and mechanistic separation of cross-presentation and endogenous antigen presentation.
    Nature Immunol, 9: 558-566, Epub Mar 30, doi:10.1038/ni.1601 (Comment in Nature Immunol 9: 461-463 & Nature Rev Immunol, Research Highlights 8)
    Press release: http://www3.uni-bonn.de/Pressemitteilungen/wie-killerzellen-auf-die-richtige-spur-kommen

  23. Eter N, Engel DR, Meyer L, Helb HM, Roth F, Holz FG, Kurts C. 2008. In vivo visualization of dendritic cells, macrophages and microglial cells responding to laser-induced damage in the posterior pole of the eye. Invest Ophthalmol Vis Sci, Epub Mar 3, doi:10.1167/iovs.07-1322

  24. Lukacs-Kornek V, Burgdorf S, Diehl L, Specht S, Kornek M, Kurts C. 2008. The kidney-renal lymph node-system contributes to cross-tolerance against innocuous circulating antigen. J Immunol, 180: 706-715

  25. Kurts C. 2008. Th17 cells: a third subset of CD4+ T effector cells involved in organ-specific autoimmunity. Nephrol Dial Transpl, 23:816-9, Epub Nov 28, 2007

  26. Kurts C, Heymann F, Lukacs-Kornek V, Scholz J, Boor P, Floege J. 2007. Role of T cells and dendritic cells in immunopathology of glomerular disease. Springer Semin Immunopathol, 29: 317-335

  27. Panzer U, Steinmetz OM, Paust HJ, Meyer-Schwesinger C, Peters A, Turner JE, Zahner G, Reichel F, Kurts C, Hopfer H, Helmchen U, Haag F, Schneider A, Stahl RAK. 2007. The chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice. J Am Soc Nephrol, 18: 2071-2084

  28. Burgdorf S, Kautz A, Böhnert V, Knolle PA, Kurts C. 2007. Distinct antigen uptake and intracellular routing mechanisms in CD4 and CD8 T cell activation. Science, 316: 612-6
    press release: http://www3.uni-bonn.de/Pressemitteilungen/vergiften-verdauen-oder-in-den-selbstmord-treiben

  29. Panzer U, Steinmetz OM, Paust HJ, Meyer-Schwesinger C, Peters A, Turner JE, Zahner G, Reichel F, Kurts C, Hopfer H, Helmchen U, Haag F, Schneider A, Stahl RAK. 2007. The chemokine receptor CXCR3 mediates T cell recruitment and tissue injury in nephrotoxic nephritis in mice. J Am Soc Nephrol, 18: 2071-2084

  30. Hänninen A, Nurmela R, Heino J; Maksimow M, Jalkanen S, Kurts C. 2007. Autoreactive T cells can use different homing mechanisms to infiltrate and destroy pancreatic islets. Am J Pathol, 170: 240-250

  31. Engel D, Dobrindt U, Tittel A, Peters P, Maurer J, Gütgemann I, Kaissling B, Kuziel W, Jung S, Kurts C. 2006. TNFa/iNOS-producing dendritic cells are rapidly recruited to the bladder in urinary tract infection, but are dispensable for bacterial clearance. Infect Immun, 74:6100-7

  32. Koscielny A, Boerner T, Wehner S, Kurts C, KAlff JC. 2006. The role of dendritic cells in the gastrointestinal field effect. Transplant Proc, 38: 1815-7

  33. Burgdorf S, Lukacs-Kornek V, Kurts C. 2006. The mannose receptor mediates uptake of soluble, but not of cell-associated antigen for cross-presentation.
    J. Immunol, 176, 76: 6770-6

  34. Benke D, Krüger T, Lang A, Hamilton-Williams EE, Kurts C. 2006.Inclusion of Brefeldin A during dendritic cell isolation allows in vitro detection of cross-presented self antigens. J Immunol Methods, 310:12-9.

  35. Hamilton-Williams EE, Lang A, Benke D, Davey GM, Wiesmüller KH, Kurts C. 2005. Cutting Edge: Toll-like receptor ligands are not sufficient to break cross-tolerance to self antigens. J Immunol, 174: 1159-1163

  36. Lang A, Benke D, Eitner F, Engel D, Ehrlich S, Breloer M, Hamilton-Williams EE, Specht S, Hoerauf A, Floege J, Bonin A, Kurts C. 2005. Heat shock protein 60 is released in immune-mediated glomerulonephritis and aggravates disease. In vivo evidence for an immunological danger signal. J Am Soc Nephrol, 16: 383-391

  37. Kruger T, Benke D, Eitner F, Lang A, Wirtz M, Hamilton-Williams EE, Engel D, Giese B, Muller-Newen G, Floege J, Kurts C. 2004. Identification and functional characterization of dendritic cells in the healthy murine kidney and in experimental glomerulonephritis. J Am Soc Nephrol, 15: 613-21

  38. Davey GM, C Kurts, JFAP Miller, P Bouillet, A Strasser, A Brooks, FR Carbone and WR Heath. 2002. Peripheral deletion of autoreactive CD8 T cells by cross-presentation of self antigen occurs by a Bcl-2-inhibitable pathway mediated by Bim. J Exp Med, 196: 947-55

  39. Kurts C, I Klebba, GM Davey, KM Koch, JFAP Miller, WR Heath, J Floege. 2001. Kidney protection against autoreactive CD8+ T cells distinct from immunoprivilege and sequestration. Kidney Int, 60: 664-71

  40. Kurts C, M Cannarile, I Klebba, T Brocker. 2001. Dendritic cells are sufficient to cross-present self antigens to CD8 T cells in vivo. J Immunol, 166: 1439-42.

  41. Kurts C. 2000. Cross-presentation: inducing CD8 T cell immunity and tolerance. J Mol Med, 6: 326-32

  42. Limmer A, J Ohl, C Kurts, HG Ljunggren, Y Reiss, M Groettrup, F Momburg, B Arnold, PA Knolle. 2000. Efficient presentation of exogenous antigen by liver endothelial cells to CD8+ T cells results in antigen-specific T-cell tolerance. Nature Med. 6: 1348-54

  43. Kurts C, R Southerland, G Davey, M Li, A Lew, E Blanas, JFAP Miller, FR Carbone, WR Heath. 1999. CD8 T cell ignorance or tolerance to islet antigens depends on antigen dose. Proc Natl Acad Sci (USA), 96: 12703-7

  44. Kurts C, FR Carbone, MF Krummel, KM Koch, JFAP Miller, WR Heath. 1999. CD30 signalling protects against CD8 T cell-mediated autoimmune diabetes. Nature, 398: 341-344

  45. Miller JFAP, C Kurts, FR Carbone, Heath WR. 1998. Induction of peripheral CD8+ T cell tolerance by cross-presentation of self antigens. Immunol Rev 165: 267-277

  46. Kurts C, L Shuo, F Köntgen, SR Holdsworth, PG Tipping. 1998. MHC class II expression by intrinsic renal cells is required for crescentic glomerulonephritis.
    J Exp Med, 188: 597-602

  47. Kurts C, WR Heath, H Kosaka, JFAP Miller, FR Carbone. 1998. The peripheral deletion of autoreactive CD8+ T cells induced by cross-presentation of self antigens involves signaling through CD95 (Fas, Apo-1). J Exp Med, 188: 415-420

  48. Kurts C, JFAP Miller, R. Subramanium, FR Carbone, WR Heath. 1998. MHC class I-restricted cross-presentation is biased towards high dose antigens and those released during cellular destruction. J Exp Med, 188: 409-414

  49. Kurts C, FR Carbone, M Barnden, E Blanas, J Allison, WR Heath, JFAP Miller. 1997. CD4+ T cell help impairs CD8+ T cell deletion induced by cross-presentation of self antigens and favors autoimmunity. J Exp Med, 186: 2057-2062

  50. Kurts C, H Kosaka, FR Carbone, JFAP Miller und WR Heath. 1997. Exogenous class I-restricted cross-presentation of self antigens can lead to deletion of autoreactive CD8+ T cells. J Exp Med, 186: 239-245

  51. Kurts C, WR Heath, FR Carbone, J Allison, JFAP Miller,  H Kosaka. 1996. Constitutive class I-restricted exogenous presentation of self antigens in vivo. J Exp Med, 184: 923-930

  52. Oppermann M, C Kurts, R Zierz, E Quentin, MH Weber,  O Götze. 1991. Elevated plasma levels of the immunosuppressive complement fragment Ba in renal failure. Kidney Int, 40: 939-947

  53. Oppermann M, H Baumgarten, E Brandt, W Gottsleben, C Kurts, O Götze. 1990. Quantitation of components of the alternative pathway of complement (APC) by enzyme-linked immunosorbent assays. J Immunol Methods, 133: 181-190

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