Journalartikel

Emerging targets of biologic therapies for rheumatoid arthritis


AutorenlisteTarner, Ingo H.; Mueller-Ladner, Ulf; Gay, Steffen

Jahr der Veröffentlichung2007

Seiten336-345

ZeitschriftNature Clinical Practice Rheumatology

Bandnummer3

Heftnummer6

ISSN1745-8382

DOI Linkhttps://doi.org/10.1038/ncprheum0506

VerlagNature Publishing Group


Abstract
Advances in molecular biology and the clinical success of strategies that target tumor necrosis factor (TNF) have led to further research into the pathophysiology of human rheumatoid arthritis. Several novel therapeutic targets have emerged from these efforts, including not only molecules that regulate TNF (e.g. TNF-alpha converting enzyme), the complex cytokine network (e.g. interleukin [IL]-6, IL-15, IL-17) and several adipokines, but also targets that originate from cellular and subcellular components of the disease. Strategies that aim at cellular targets include antibodies to CD20 or BLyS (also known as TNF ligand family member 13b), which deplete or inhibit B cells, as well as approaches that interfere with membrane-derived microparticles. Components of subcellular pathways, which are predominantly upstream of the central regulator of transcription nuclear factor kappa B, have also been studied. Of these, strategies that target mitogen-activated protein kinases have a leading role and are on the verge of clinical use; approaches that target specific molecules such as Janus kinases, signal transducer and activator of transcription proteins, and suppressor of cytokine signaling proteins also seem to show promise and might have a clinical application in the future.



Zitierstile

Harvard-ZitierstilTarner, I., Mueller-Ladner, U. and Gay, S. (2007) Emerging targets of biologic therapies for rheumatoid arthritis, NATURE CLINICAL PRACTICE RHEUMATOLOGY, 3(6), pp. 336-345. https://doi.org/10.1038/ncprheum0506

APA-ZitierstilTarner, I., Mueller-Ladner, U., & Gay, S. (2007). Emerging targets of biologic therapies for rheumatoid arthritis. NATURE CLINICAL PRACTICE RHEUMATOLOGY. 3(6), 336-345. https://doi.org/10.1038/ncprheum0506



Schlagwörter


biologicsCOLLAGEN-INDUCED ARTHRITISDESTRUCTIONDOUBLE-BLINDJOINT INFLAMMATIONMICROPARTICLESMONOCLONAL-ANTIBODYT-CELL ACTIVATION


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