IL-17 derived from juxta-articular bone and synovium contributes to joint degradation in rheumatoid arthritisReportar como inadecuado




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Arthritis Research and Therapy

, 3:168

First Online: 26 January 2001Received: 02 October 2000Revised: 15 November 2000Accepted: 19 December 2000

Abstract

The origin and role of IL-17, a T-cell derived cytokine, in cartilage and bone destruction during rheumatoid arthritis RA remain to be clarified. In human ex vivo models, addition of IL-17 enhanced IL-6 production and collagen destruction, and inhibited collagen synthesis by RA synovium explants. On mouse cartilage, IL-17 enhanced cartilage proteoglycan loss and inhibited its synthesis. On human RA bone explants, IL-17 also increased bone resorption and decreased formation. Addition of IL-1 in these conditions increased the effect of IL-17. Blocking of bone-derived endogenous IL-17 with specific inhibitors resulted in a protective inhibition of bone destruction. Conversely, intra-articular administration of IL-17 into a normal mouse joint induced cartilage degradation. In conclusion, the contribution of IL-17 derived from synovium and bone marrow T cells to joint destruction suggests the control of IL-17 for the treatment of RA.

Keywordsbone cartilage degradation IL-17 rheumatoid arthritis AbbreviationsCTXC-terminal collagen cross-links

ELISAenzyme-linked immunosorbent assay

GM-CSFgranulocyte–monocyte colony stimulating factor

IGF-1insulin-like growth factor

mAbmonoclonal antibody

PGproteoglycan

PICPC-propeptide of type I collagen

RArheumatoid arthri-tis

sIL-17Rsoluble IL-17 receptor

TNFtumor necrosis factor.

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Autor: Martine Chabaud - Erik Lubberts - Leo Joosten - Wim van den Berg - Pierre Miossec

Fuente: https://link.springer.com/







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