2004
DOI: 10.1111/j.1365-2133.2004.05960.x
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Abstract: Tumour necrosis factor (TNF)-alpha is thought to play a major role in the pathophysiology of psoriasis. Good clinical responses of psoriasis to anti-TNF-alpha-based therapies have recently been demonstrated. We studied the effect of infliximab, a monoclonal antibody against TNF-alpha, on chemokine expression in pustular psoriasis. A 61-year-old man with a 2-year history of severe pustular psoriasis of von Zumbusch type who did not respond to conventional therapies responded rapidly to treatment with infliximab… Show more

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Cited by 61 publications
(51 citation statements)
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“…Etanercept competitively binds TNF-␣ and TNF-␤. 6,7 Cases of leukocytolytic vasculitis, urticarial rash, pancytopenia, and aplastic anemia have been reported with etanercept use. [8][9][10] In addition, patients are susceptible to opportunistic infections and reactivation of tuberculosis.…”
Section: Commentmentioning
confidence: 99%
“…Etanercept competitively binds TNF-␣ and TNF-␤. 6,7 Cases of leukocytolytic vasculitis, urticarial rash, pancytopenia, and aplastic anemia have been reported with etanercept use. [8][9][10] In addition, patients are susceptible to opportunistic infections and reactivation of tuberculosis.…”
Section: Commentmentioning
confidence: 99%
“…Clinical improvements of psoriasis associate with a fall in lesional skin and serum TNF-· levels (36,56,57), whereas clinical aggravations of psoriatic area severity index (PASI) scores concur with surges in serum and lesional skin TNF-· concentrations (40,60). Neutralisation of TNF-· by infliximab, an anti-TNF-·-specific chimerical monoclonal antibody, or by etanercept, a soluble p75 TNF receptor fusion protein that binds both TNF and lymphotoxin (LT), is known to cause a rapid and complete remission of psoriasis even in its recalcitrant von Zumbusch form (39)(40)(41) and, when associated with methotrexate, of psoriatic arthritis (58)(59)(60)(61).…”
Section: Discussionmentioning
confidence: 99%
“…Resident dermal cells (fibroblasts, mast-cells) and infiltrated antigen-presenting cells (APCs), macrophages, and T lymphocytes also express TNF-· (38). The early-occurring TNF-· overproduction and hyper-secretion in psoriasis vulgaris, and in its recalcitrant generalised pustular (von Zumbusch) form (39)(40)(41) favours the cellular infiltration of epidermal and dermal layers by eliciting the expression of intercellular adhesion molecules such as ICAM-1, V-CAM-1, and E-selectin by the keratinocytes and endothelial cells (42). In synergism with IFN-Á and IL-1, TNF-· acts as a proinflammatory agent by up-regulating cytokines and chemokines such as IL-8 (19,20,43), IL-6, IL-1, leukemia inhibitory factor (LIF), GM-CSF (43), and TGF-· (19).…”
Section: Introductionmentioning
confidence: 99%
“…Amongst them, proinflammatory and immunomodulatory cytokines TNF alpha and interferon gamma are the principal. The chemokine expression is downmodulated by some drugs including cyclosporine A, corticosteroids, vitamin D3 analog tacalcitol, or anti-TNF alpha biological therapy (2,6,11,18), all of which are used in the treatment and having therapeutical effect in psoriasis. The level of RANTES is negatively influenced by UV-B irradiation which is an integral part of GT (4).…”
Section: Discussionmentioning
confidence: 99%