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The NCBI web site requires JavaScript to function. Psoriasis vulgaris is a chronic inflammatory skin disease that results from the complex interplay between http://festival-celle.de/symptome-der-psoriasis-auf-dem-gesicht-foto.php, dendritic cells, and T cells. Keratinocytes trigger innate and adaptive immune responses.

Dermal myeloid dendritic Rockefeller Psoriasis regulate T cell activation and production of cytokines and chemokines that amplify inflammation. The initiation phase of psoriasis involves Toll-like receptors, read article peptide LL37, and plasmacytoid dendritic cells. Keratinocytes are the main cutaneous cell type expressing IL receptors and hence the click at this page circuit is amplified by keratinocytes upregulating mRNAs for a range of inflammatory products.

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Add to My Bibliography. Generate a file for use with external citation management software. See comment in Rockefeller Psoriasis Commons below Dermatol Clin.

Kim J 1Krueger JG 2. Author information 1 Laboratory for Investigative Dermatology, The Rockefeller University, York Ave, New York, NYUSA. Abstract Psoriasis vulgaris is a chronic inflammatory skin disease that results from the complex interplay between keratinocytes, dendritic cells, and T cells.

Dendritic cells; Immunology; Immunopathogenesis; Keratinocyte; Psoriasis; T cells. Publication types, MeSH terms, Substances, Grant support Publication types Research Support, N. LinkOut - more resources Full Text Sources Elsevier Science W. Saunders ClinicalKey Medical ClinicalTrials. PubMed Commons home PubMed Commons. How to cite this comment: Supplemental Rockefeller Psoriasis Full text links.

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