Anti-TNF therapy: Where have we got to in 2005?

Feldmann, Marc; Brennan, Fionula M.; Foxwell, Brian M. J.; Taylor, Peter; Williams, Richard O.; Maini, R N

doi:10.1016/j.jaut.2005.09.006

Cited by 88 publications

(61 citation statements)

References 27 publications

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“…These drugs have had a major impact on the treatment of rheumatoid arthritis (RA) but they are expensive, have to be injected and are only partially effective (only have the desired effect in 50% of patients) (Feldmann et al, 2005). For these reasons, there is undiminished interest in identifying novel, orally active compounds that block the production of TNF␣.…”

Section: Introductionmentioning

confidence: 99%

TPL2-mediated activation of ERK1 and ERK2 regulates the processing of pre-TNFα in LPS-stimulated macrophages

Rousseau

Papoutsopoulou²,

Symons³

et al. 2008

Journal of Cell Science

121

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unaffected by inhibition of the TPL2-MKK1/2-ERK1/2 pathway. Finally, we show that TACE, the protease that cleaves pre-TNF␣ to secreted TNF␣, is phosphorylated by ERK1 and ERK2 (ERK1/2) at Thr735 in LPS-stimulated macrophages. Therefore, although TACE activity per se is not required for the LPS-stimulated cell surface expression of pre-TNF␣, the phosphorylation of this protease might contribute to, or be required for, the cell surface expression of the pre-TNF␣-TACE complex.

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Section: Introductionmentioning

confidence: 99%

TPL2-mediated activation of ERK1 and ERK2 regulates the processing of pre-TNFα in LPS-stimulated macrophages

Rousseau

Papoutsopoulou²,

Symons³

et al. 2008

Journal of Cell Science

121

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“…Our study shows that primary human monocytes are responsive to PBEF, suggesting that PBEF acts in an autocrine manner to increase serum levels. Notably, activation of monocytes by PBEF results in the production TNF␣, a key cytokine in the pathogenesis of RA (27). Moreover, PBEF present in synovial fluid might trigger chronic inflammation not only via induction of proinflammatory cytokine production by RASFs but also by a direct antiapoptotic effect on neutrophils (10).…”

Section: Discussionmentioning

confidence: 99%

Pre–B cell colony‐enhancing factor/visfatin, a new marker of inflammation in rheumatoid arthritis with proinflammatory and matrix‐degrading activities

Brentano

Schorr

Ospelt

et al. 2007

Arthritis & Rheumatism

238

216

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Objective. To study possible mechanisms that mediate induction of the recently described adipocytokine pre-B cell colony-enhancing factor (PBEF) in joints of patients with rheumatoid arthritis (RA), and to analyze whether levels of PBEF correlate with disease severity and whether PBEF itself has the potential to act as a proinflammatory and destructive mediator in RA.Methods. RA synovial fibroblasts (RASFs) and monocytes were stimulated with Toll-like receptor (TLR) ligands, cytokines, and recombinant human PBEF or were transfected with PBEF expression constructs or with PBEF-specific small interfering RNA. Production of interleukin-6 (IL-6), IL-8, and tumor necrosis factor ␣ (TNF␣) was measured by enzymelinked immunosorbent assay, and expression of matrix metalloproteinases (MMPs) was assessed by real-time polymerase chain reaction. PBEF expression in synovial tissue, synovial fluid, serum, and SFs was assessed by immunohistochemistry, in situ hybridization, Western blotting, and enzyme immunoassays. Results. In RASFs, PBEF was up-regulated by

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“…tumor necrosis factor (TNF) has been demonstrated to play a key role in the pathologic processes of RA (1)(2)(3)(4)(5). In the murine model of collagen-induced arthritis (CIA), it was shown that neutralizing TNF ameliorated CIA, especially when treatment was started before or early after the onset of disease (6).…”

mentioning

confidence: 99%

“…In the murine model of collagen-induced arthritis (CIA), it was shown that neutralizing TNF ameliorated CIA, especially when treatment was started before or early after the onset of disease (6). Importantly, neutralizing TNF in RA patients considerably improves joint inflammation and inhibits the progression of joint destruction (1)(2)(3)(4)(5). This led to use of the first anti-TNF biologic agents, for the treatment of RA.…”

mentioning

confidence: 99%

Tumor necrosis factor–interleukin‐17 interplay induces S100A8, interleukin‐1β, and matrix metalloproteinases, and drives irreversible cartilage destruction in murine arthritis: Rationale for combination treatment during arthritis

Koenders¹,

Marijnissen²,

Devesa³

et al. 2011

Arthritis & Rheumatism

131

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Objective. To examine whether synovial interleukin-17 (IL-17) expression promotes tumor necrosis factor (TNF)-induced joint pathologic processes in vivo, and to analyze the surplus ameliorative value of neutralizing IL-17 in addition to TNF during collageninduced arthritis (CIA).Methods. Adenoviral vectors were used to induce overexpression of IL-17 and/or TNF in murine knee joints. In addition, mice with CIA were treated, at different stages of arthritis, with soluble IL-17 receptor (sIL-17R), TNF binding protein (TNFBP), or the combination.Results. Overexpression of IL-17 and TNF resulted in joint inflammation and bone erosion in murine knees. Interestingly, IL-17 strikingly enhanced both the joint-inflammatory and joint-destructive capacity of TNF. Further analysis revealed a strongly enhanced up-regulation of S100A8, IL-1␤, and matrix metalloproteinase (MMP) messenger RNA, only when both TNF and IL-17 were present. Moreover, the increase in irreversible cartilage destruction was not merely the result of enhanced inflammation, but also was associated with a direct synergistic effect of these cytokines in the joint. S100A9 deficiency in mice protected against IL-17/TNF-induced expression of cartilage NITEGE neoepitopes. During established arthritis, the combination of sIL-17R and TNFBP was more effective than the anticytokine treatments alone, and significantly inhibited further joint inflammation and cartilage destruction.Conclusion. Local synovial IL-17 expression enhances the role of TNF in joint destruction. Synergy between TNF and IL-17 in vivo results in striking exaggeration of cartilage erosion, in parallel with a synergistic up-regulation of S100A8, IL-1␤, and erosive MMPs. Moreover, neutralizing IL-17 in addition to TNF further improves protection against joint damage and is still effective during late-stage CIA. Therefore, compared with anti-TNF alone, combination blocking of TNF and IL-17 may have additional therapeutic value for the treatment of destructive arthritis.Rheumatoid arthritis (RA) is a chronic disorder with unknown etiology. It is characterized by autoimmunity, infiltration of joint synovium by activated inflammatory cells, synovial hyperplasia, and progressive destruction of cartilage and bone. In the last decade, Supported by grants from the Dutch Arthritis Association (NR 00-1-302) and from the Stichting De Drie Lichten,

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Anti-TNF therapy: Where have we got to in 2005?

Cited by 88 publications

References 27 publications

TPL2-mediated activation of ERK1 and ERK2 regulates the processing of pre-TNFα in LPS-stimulated macrophages

TPL2-mediated activation of ERK1 and ERK2 regulates the processing of pre-TNFα in LPS-stimulated macrophages

Pre–B cell colony‐enhancing factor/visfatin, a new marker of inflammation in rheumatoid arthritis with proinflammatory and matrix‐degrading activities

Tumor necrosis factor–interleukin‐17 interplay induces S100A8, interleukin‐1β, and matrix metalloproteinases, and drives irreversible cartilage destruction in murine arthritis: Rationale for combination treatment during arthritis

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