Asset Details
Do you wish to reserve the book?
Psoriasiform dermatitis is driven by IL-36–mediated DC-keratinocyte crosstalk
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Psoriasiform dermatitis is driven by IL-36–mediated DC-keratinocyte crosstalk
Do you wish to request the book?
Psoriasiform dermatitis is driven by IL-36–mediated DC-keratinocyte crosstalk
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Psoriasiform dermatitis is driven by IL-36–mediated DC-keratinocyte crosstalk
2012
Overview
Psoriasis is a chronic inflammatory disorder of the skin affecting approximately 2% of the world's population. Accumulating evidence has revealed that the IL-23/IL-17/IL-22 pathway is key for development of skin immunopathology. However, the role of keratinocytes and their crosstalk with immune cells at the onset of disease remains poorly understood. Here, we show that IL-36R-deficient (Il36r-/-) mice were protected from imiquimod-induced expansion of dermal IL-17-producing γδ T cells and psoriasiform dermatitis. Furthermore, IL-36R antagonist-deficient (Il36rn-/-) mice showed exacerbated pathology. TLR7 ligation on DCs induced IL-36-mediated crosstalk with keratinocytes and dermal mesenchymal cells that was crucial for control of the pathological IL-23/IL-17/IL-22 axis and disease development. Notably, mice lacking IL-23, IL-17, or IL-22 were less well protected from disease compared with Il36r-/- mice, indicating an additional distinct activity of IL-36 beyond induction of the pathological IL-23 axis. Moreover, while the absence of IL-1R1 prevented neutrophil infiltration, it did not protect from acanthosis and hyperkeratosis, demonstrating that neutrophils are dispensable for disease manifestation. These results highlight a central and unique IL-1-independent role for IL-36 in control of the IL-23/IL-17/IL-22 pathway and development of psoriasiform dermatitis.
Publisher
American Society for Clinical Investigation
Subject
/ Cell Communication - genetics
/ Cell Communication - immunology
/ Dendritic Cells - immunology
/ Dendritic Cells - metabolism
/ Disease
/ Membrane Glycoproteins - genetics
/ Membrane Glycoproteins - immunology
/ Membrane Glycoproteins - metabolism
/ Mice
/ Receptors, Interleukin-1 - genetics
/ Receptors, Interleukin-1 - immunology
/ Receptors, Interleukin-1 - metabolism
/ Skin
/ Toll-Like Receptor 7 - genetics
/ Toll-Like Receptor 7 - immunology
