Journal
JOURNAL OF IMMUNOLOGY
Volume 185, Issue 10, Pages 5688-5691Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1001538
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Funding
- Wellcome Trust [GR078173MA]
- National Institutes of Health [RO1AR040065]
- Medical Research Council UK [G0601387]
- Dunhill Medical Trust
- Bonizzi-Theler Foundation
- Hermann Klaus Foundation
- Hartmann Muller Foundation
- Schering-Plough Biopharma/Merck Research Laboratories
- Department of Health via the National Institute for Health Research
- Medical Research Council [G0601387, G0600698B] Funding Source: researchfish
- MRC [G0601387] Funding Source: UKRI
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Interleukin-23 is a key cytokine involved in the generation of Th17 effector cells. Clinical efficacy of an anti-p40 mAb blocking both IL-12 and IL-23 and disease association with single nucleotide polymorphisms in the IL23R gene raise the question of a functional role of IL-23 in psoriasis. In this study, we provide a comprehensive analysis of IL-23 and its receptor in psoriasis and demonstrate its functional importance in a disease-relevant model system. The expression of IL-23 and its receptor was increased in the tissues of patients with psoriasis. Injection of a mAb specifically neutralizing human IL-23 showed IL-23-dependent inhibition of psoriasis development comparable to the use of anti-TNF blockers in a clinically relevant xenotransplant mouse model of psoriasis. Together, our results identify a critical functional role for IL-23 in psoriasis and provide the rationale for new treatment strategies in chronic epithelial inflammatory disorders. The Journal of Immunology, 2010, 185: 5688-5691.
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