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Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation
Published on: December 26, 2017
Could anti IL12/23 therapy replace anti-TNF biologics?
Marius A Ionescu1, Jasna Lipozencić
1Dermatology Polyclinic Saint-Louis Hospital 1, Avenue Claude Vellefaux, 75010 Paris, France. marius.ionescu@club-internet.fr
Abstract:
Biologic therapies improved dramatically the outcome of psoriatic arthritis and moderate to severe chronic plaque psoriasis. Anti-TNF agents were developed approximately one decade ago by rheumatologists and today represent one of the most effective classes of drugs in severe psoriasis resistant to 2 out of 3 "classic" systemic therapies (methotrexate, cyclosporine, and PUVA). Recent studies on psoriasis pathogenesis were focused on early steps of the inflammatory cascade, i.e. activation of T cells with a recently described phenotype Th17 and consequent expression of interleukins (IL) 12 and 23. IL12 and IL23 have a common p40 subunit that is a target of a new therapeutic class, fully human monoclonal antibodies anti IL12/23: ustekinumab and ABT-874. Randomized, placebo-controlled clinical trials in patients with moderate to severe chronic plaque psoriasis using ustekinumab and ABT-874 showed PASI 75 achievements at week 12 in 80% and 93% of patients, respectively. Larger studies are ongoing in order to assess the safety profile of this new therapy. As anti-TNF drugs represent an important and effective treatment of psoriatic arthritis and moderate to severe plaque psoriasis, comparative studies are needed to assess the advantages, the safety and the place of anti-IL12/23 in the era of biologic therapy.
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