CD1a on Langerhans cells controls inflammatory skin diseases

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CD1a on Langerhans cells controls inflammatory skin diseases

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Title: CD1a on Langerhans cells controls inflammatory skin diseases
Author: Kim, Ji Hyung; Hu, Yu; Yongqing, Tang; Kim, Jessica; Hughes, Victoria A.; Nours, Jérôme Le; Marquez, Elsa A.; Purcell, Anthony W.; Wan, Qi; Sugita, Masahiko; Rossjohn, Jamie; Winau, Florian

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Citation: Kim, J. H., Y. Hu, T. Yongqing, J. Kim, V. A. Hughes, J. L. Nours, E. A. Marquez, et al. 2016. “CD1a on Langerhans cells controls inflammatory skin diseases.” Nature immunology 17 (10): 1159-1166. doi:10.1038/ni.3523. http://dx.doi.org/10.1038/ni.3523.
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Abstract: CD1a is a lipid-presenting molecule abundantly expressed on Langerhans cells. However, the in vivo role of CD1a remains unclear, principally because CD1a is lacking in mice. Using CD1a-transgenic mice, we show that the plant-derived lipid urushiol triggers CD1a-dependent skin inflammation, driven by CD4+ T cells producing IL-17 and IL-22. Human subjects with poison ivy dermatitis showed a similar cytokine signature following CD1a-mediated urushiol recognition. Among different urushiol congeners, we identified diunsaturated pentadecylcatechol (C15:2) as the dominant antigen for CD1a-restricted T cells. We determined the crystal structure of the CD1a-urushiol (C15:2) complex, demonstrating the molecular basis of urushiol interaction with the antigen-binding cleft of CD1a. In a mouse model and psoriasis patients, CD1a amplified inflammatory responses mediated by TH17 cells reactive with self lipid antigens. Treatment with blocking antibodies against CD1a alleviated skin inflammation. Thus, we propose CD1a as a potential therapeutic target in inflammatory skin diseases.
Published Version: doi:10.1038/ni.3523
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5791155/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:34868780
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