Suppression of the cutaneous immune response following topical application of the prostaglandin PGE2 |
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| Authors: | L A Rheins L Barnes S Amornsiripanitch C E Collins J J Nordlund |
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| Institution: | 1. Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi''an, China;2. Department of Transfusion Medicine, Xijing Hospital, Fourth Military Medical University, Xi''an, China;3. Department of Microbiology, School of Basic Medicine, Fourth Military Medical University, Xi''an, China;1. Department of Allergy and Rheumatology, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing 210042, China;2. Department of Dermatology, Huashan Hospital, Fudan University, Shanghai 200040, China;3. Gene Editing Laboratory, Texas Heart Institute, Houston, Texas 77030, USA;4. Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China;5. Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518052, China;1. Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China;2. Division of Joint Surgery and Sports Medicine, Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China;3. Department of Women Health Care, Hubei Women & Children’s Hospital, Wuhan, China;4. Department of Urology, The Central Hospital of Wuhan, Wuhan, China |
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| Abstract: | UVB irradiation (290-320 nm) and topical applications of arachidonic acid (AA) in mice decrease the number of identifiable Langerhans cells and alter the cutaneous immune response. Application of contact allergens such as dinitrofluorobenzene (DNFB) to irradiated or AA-treated skin induces antigen-specific tolerance. Indomethacin (IM), a cyclooxygenase inhibitor, administered orally to mice prior to UVB irradiation or prior to the topical application of arachidonic acid, abrogates suppression of contact hypersensitivity (CHS) to DNFB. This suggests a byproduct of arachidonic acid generated through the cyclooxygenase pathway may be involved in the immune suppression. Topical application of various prostaglandins (PGE2, PGD2, PGF2 alpha, and CTXA2) did not cause alterations in the population density of the identifiable Ia+ dendritic Langerhans cells. PGE2, but no other tested agent, produced a suppression of the CHS response to DNFB. These observations suggests that of the various prostaglandins, PGE2 might be one of several biochemical signals which mediate the suppression of contact hypersensitivity reactions following ultraviolet radiation exposure. However, the mechanisms by which PGE2 produces its suppressive effects have not been identified. |
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