Abstract |
Psoriasis is an instructive example highlighting our growing knowledge about pathophysiological functions of interleukin (IL)-17. IL-17A is the predominant isoform implicated in key pathogenic features in this and other chronic inflammatory disorders. Several monoclonal antibodies targeting IL-17A ( secukinumab, ixekizumab) or its IL-17RC/RA receptor ( brodalumab) are currently in late stages of clinical development, where they have shown impressive efficacy. While the eponymous IL-17 has been thought to originate primarily from T helper (Th)17 cells, more recent investigations by several groups suggest that other cell types in psoriatic lesions, such as neutrophils and mast cells, are rich sources of IL-17, thus presumably contributing to the disease process to an as yet underestimated extent. This recent paradigm shift provides a plausible explanation for the rapid and strong efficacy of the novel compounds targeting IL-17 functions in psoriasis and other inflammatory disorders, and provide a more comprehensive view on the complex cytokine network in these conditions.
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Authors | Michael P Schön |
Journal | Experimental dermatology
(Exp Dermatol)
Vol. 23
Issue 11
Pg. 804-6
(Nov 2014)
ISSN: 1600-0625 [Electronic] Denmark |
PMID | 25219805
(Publication Type: Journal Article, Review, Comment)
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Copyright | © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. |
Chemical References |
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Topics |
- Animals
- Gene Expression Regulation
- Humans
- Interleukin-17
(immunology)
- Mast Cells
(immunology)
- Neutrophils
(immunology)
- Psoriasis
(immunology)
- T-Lymphocyte Subsets
(immunology)
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