Seemayer, C. A. ; Distler, O. ; Kuchen, S. ; Müller-Ladner, U. ; Michel, B. A. ; Neidhart, M. ; Gay, R. E. ; Gay, S.
Alternative Links zum Volltext:DOIVerlag
| Dokumentenart: | Artikel |
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| Titel eines Journals oder einer Zeitschrift: | Zeitschrift f�r Rheumatologie |
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| Verlag: | SPRINGER HEIDELBERG |
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| Ort der Veröffentlichung: | HEIDELBERG |
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| Band: | 60 |
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| Nummer des Zeitschriftenheftes oder des Kapitels: | 5 |
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| Seitenbereich: | S. 309-318 |
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| Datum: | 2001 |
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| Institutionen: | Medizin > Lehrstuhl für Innere Medizin I |
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| Identifikationsnummer: | | Wert | Typ |
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| 10.1007/s003930170030 | DOI |
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| Stichwörter / Keywords: | INTERLEUKIN-1 RECEPTOR ANTAGONIST; MESSENGER-RNA EXPRESSION; TUMOR-SUPPRESSOR GENE; MATRIX METALLOPROTEINASES; DIFFERENTIAL EXPRESSION; BCL-2 EXPRESSION; GROWTH-FACTOR; CATHEPSIN-B; T-CELLS; IN-SITU; rheumatoid arthritis; synovial fibroblasts |
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| Dewey-Dezimal-Klassifikation: | 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin |
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| Status: | Veröffentlicht |
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| Begutachtet: | Ja, diese Version wurde begutachtet |
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| An der Universität Regensburg entstanden: | Ja |
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| Dokumenten-ID: | 73438 |
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Web of Science
Zusammenfassung
Rheumatoid arthritis (RA) is a chronic inflammatory disease, which is mainly characterized by synovial hyperplasia, pathological immune phenomena and progressive destruction of the affected joints. Various cell types are involved in the pathogenesis of RA including T cells, antigen presenting cells, and endothelial cells. Recent experimental evidence suggests that the CD40/CD154 system might play ...
Zusammenfassung
Rheumatoid arthritis (RA) is a chronic inflammatory disease, which is mainly characterized by synovial hyperplasia, pathological immune phenomena and progressive destruction of the affected joints. Various cell types are involved in the pathogenesis of RA including T cells, antigen presenting cells, and endothelial cells. Recent experimental evidence suggests that the CD40/CD154 system might play an important role in the development of RA. Our experimental approach focuses on RA synovial fibroblasts (RA-SF) that are able to destroy articular cartilage independent of inflammation. To elucidate the specific role of those cells in RA pathophysiology the following questions are currently addressed: 1. Which mechanisms do activate the RA-SF? 2. How do the activated RA-SF attach to the cartilage? 3. How do RA-SF destroy cartilage and bone?
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