Journalartikel
Autorenliste: Tarner, Ingo H.; Mueller-Ladner, Ulf; Gay, Steffen
Jahr der Veröffentlichung: 2007
Seiten: 336-345
Zeitschrift: Nature Clinical Practice Rheumatology
Bandnummer: 3
Heftnummer: 6
ISSN: 1745-8382
DOI Link: https://doi.org/10.1038/ncprheum0506
Verlag: Nature 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-Zitierstil: Tarner, 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-Zitierstil: Tarner, 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
biologics; COLLAGEN-INDUCED ARTHRITIS; DESTRUCTION; DOUBLE-BLIND; JOINT INFLAMMATION; MICROPARTICLES; MONOCLONAL-ANTIBODY; T-CELL ACTIVATION