TY - JOUR
T1 - Interleukin-1β and interleukin-6 in arthritis animal models
T2 - Roles in the early phase of transition from acute to chronic inflammation and relevance for human rheumatoid arthritis
AU - Ferraccioli, Gianfranco
AU - Bracci-Laudiero, Luisa
AU - Alivernini, Stefano
AU - Gremese, Elisa
AU - Tolusso, Barbara
AU - de Benedetti, Fabrizio
PY - 2010/11
Y1 - 2010/11
N2 - Tumor necrosis factor-α (TNF-α) is the major target of the therapeutic approach in rheumatoid arthritis. A key issue in the approach to chronic arthritis is the understanding of the crucial molecules driving the transition from the acute phase to the chronic irreversible phase of the disease. In this review we analyzed five experimental arthritis animal models (antigen-induced arthritis, adjuvant-induced arthritis, streptococcal cell wall arthritis, collagen-induced arthritis and SKG) considered as possible scenarios to facilitate interpretation of the biology of human rheumatoid arthritis. The SKG model is strictly dependent on interleukin (IL)-6. In the other models, IL-1β and IL-6, more than TNF-α, appear to be relevant in driving the transition, which suggests that these should be the targets of an early intervention to stop the course toward the chronic form of the disease.
AB - Tumor necrosis factor-α (TNF-α) is the major target of the therapeutic approach in rheumatoid arthritis. A key issue in the approach to chronic arthritis is the understanding of the crucial molecules driving the transition from the acute phase to the chronic irreversible phase of the disease. In this review we analyzed five experimental arthritis animal models (antigen-induced arthritis, adjuvant-induced arthritis, streptococcal cell wall arthritis, collagen-induced arthritis and SKG) considered as possible scenarios to facilitate interpretation of the biology of human rheumatoid arthritis. The SKG model is strictly dependent on interleukin (IL)-6. In the other models, IL-1β and IL-6, more than TNF-α, appear to be relevant in driving the transition, which suggests that these should be the targets of an early intervention to stop the course toward the chronic form of the disease.
UR - http://www.scopus.com/inward/record.url?scp=78149236392&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=78149236392&partnerID=8YFLogxK
U2 - 10.2119/molmed.2010.00067
DO - 10.2119/molmed.2010.00067
M3 - Article
C2 - 20683549
AN - SCOPUS:78149236392
VL - 16
SP - 552
EP - 557
JO - Molecular Medicine
JF - Molecular Medicine
SN - 1076-1551
IS - 11-12
ER -