Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (37)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kobold, A.
Right arrow Articles by Kallenberg, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kobold, A.
Right arrow Articles by Kallenberg, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrology Dialysis Transplantation, Vol 14, Issue 6 1366-1375, Copyright © 1999 by Oxford University Press

ORIGINAL ARTICLES

Molecular basis of renal disease. Pathophysiology of ANCA-associated glomerulonephritis

A Kobold, Y van der Geld, P Limburg, J Tervaert and C Kallenberg
Departments of Clinical Immunology and Rheumatology, University Hospital Groningen, PO Box 30001, 9700 RB Groningen, The Netherlands; Corresponding author

Key words: ANCA; glomerulonephritis; vasculitis; pathophysiology; neutrophil
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 CVIHome page
A. Uehara, Y. Hirabayashi, and H. Takada
Antibodies to Proteinase 3 Prime Human Oral, Lung, and Kidney Epithelial Cells To Secrete Proinflammatory Cytokines upon Stimulation with Agonists to Various Toll-Like Receptors, NOD1, and NOD2
Clin. Vaccine Immunol., July 1, 2008; 15(7): 1060 - 1066.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
K. Hattar, S. van Burck, A. Bickenbach, U. Grandel, U. Maus, J. Lohmeyer, E. Csernok, T. Hartung, W. Seeger, F. Grimminger, et al.
Anti-proteinase 3 antibodies (c-ANCA) prime CD14-dependent leukocyte activation
J. Leukoc. Biol., October 1, 2005; 78(4): 992 - 1000.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
M. Pederzoli, C. Kantari, V. Gausson, S. Moriceau, and V. Witko-Sarsat
Proteinase-3 Induces Procaspase-3 Activation in the Absence of Apoptosis: Potential Role of this Compartmentalized Activation of Membrane-Associated Procaspase-3 in Neutrophils
J. Immunol., May 15, 2005; 174(10): 6381 - 6390.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
S. Durant, M. Pederzoli, Y. Lepelletier, S. Canteloup, P. Nusbaum, P. Lesavre, and V. Witko-Sarsat
Apoptosis-induced proteinase 3 membrane expression is independent from degranulation
J. Leukoc. Biol., January 1, 2004; 75(1): 87 - 98.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
A. A. Rarok, P. C. Limburg, and C. G. M. Kallenberg
Neutrophil-activating potential of antineutrophil cytoplasm autoantibodies
J. Leukoc. Biol., July 1, 2003; 74(1): 3 - 15.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
Y. M. van der Geld, P. C. Limburg, and C. G. M. Kallenberg
Proteinase 3, Wegener's autoantigen: from gene to antigen
J. Leukoc. Biol., February 1, 2001; 69(2): 177 - 190.
[Abstract] [Full Text]

Home page
 Ann Rheum DisHome page
H. Locht, T. Skogh, and A. Wiik
Characterisation of autoantibodies to neutrophil granule constituents among patients with reactive arthritis, rheumatoid arthritis, and ulcerative colitis
Ann Rheum Dis, November 1, 2000; 59(11): 898 - 903.
[Abstract] [Full Text]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.