TWEAK/Fn14 Activation Participates in Skin Inflammation
Tumor necrosis factor- (TNF-) like weak inducer of apoptosis (TWEAK) participates in multiple biological activities via binding to its sole receptor—fibroblast growth factor-inducible 14 (Fn14). The TWEAK/Fn14 signaling pathway is activated in skin inflammation and modulates the inflammatory respons...
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2017/6746870 |
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| _version_ | 1849695794747146240 |
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| author | Qilu Liu Shengxiang Xiao Yumin Xia |
| author_facet | Qilu Liu Shengxiang Xiao Yumin Xia |
| author_sort | Qilu Liu |
| collection | DOAJ |
| description | Tumor necrosis factor- (TNF-) like weak inducer of apoptosis (TWEAK) participates in multiple biological activities via binding to its sole receptor—fibroblast growth factor-inducible 14 (Fn14). The TWEAK/Fn14 signaling pathway is activated in skin inflammation and modulates the inflammatory responses of keratinocytes by activating nuclear factor-κB signals and enhancing the production of several cytokines, including interleukins, monocyte chemotactic protein-1, RANTES (regulated on activation, normal T cell expressed and secreted), and interferon gamma-induced protein 10. Mild or transient TWEAK/Fn14 activation contributes to tissular repair and regeneration while excessive or persistent TWEAK/Fn14 signals may lead to severe inflammatory infiltration and tissue damage. TWEAK also regulates cell fate of keratinocytes, involving the function of Fn14-TNF receptor-associated factor-TNF receptor axis. By recruiting inflammatory cells, promoting cytokine production, and regulating cell fate, TWEAK/Fn14 activation plays a pivotal role in the pathogenesis of various skin disorders, such as psoriasis, atopic dermatitis, cutaneous vasculitis, human papillomavirus infection and related skin tumors, and cutaneous autoimmune diseases. Therefore, the TWEAK/Fn14 pathway may be a potential target for the development of novel therapeutics for skin inflammatory diseases. |
| format | Article |
| id | doaj-art-ce3e28e77a8c4c5281387dc747cb77ba |
| institution | DOAJ |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-ce3e28e77a8c4c5281387dc747cb77ba2025-08-20T03:19:39ZengWileyMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/67468706746870TWEAK/Fn14 Activation Participates in Skin InflammationQilu Liu0Shengxiang Xiao1Yumin Xia2Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi’an Jiaotong University, Xi’an, ChinaDepartment of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi’an Jiaotong University, Xi’an, ChinaDepartment of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi’an Jiaotong University, Xi’an, ChinaTumor necrosis factor- (TNF-) like weak inducer of apoptosis (TWEAK) participates in multiple biological activities via binding to its sole receptor—fibroblast growth factor-inducible 14 (Fn14). The TWEAK/Fn14 signaling pathway is activated in skin inflammation and modulates the inflammatory responses of keratinocytes by activating nuclear factor-κB signals and enhancing the production of several cytokines, including interleukins, monocyte chemotactic protein-1, RANTES (regulated on activation, normal T cell expressed and secreted), and interferon gamma-induced protein 10. Mild or transient TWEAK/Fn14 activation contributes to tissular repair and regeneration while excessive or persistent TWEAK/Fn14 signals may lead to severe inflammatory infiltration and tissue damage. TWEAK also regulates cell fate of keratinocytes, involving the function of Fn14-TNF receptor-associated factor-TNF receptor axis. By recruiting inflammatory cells, promoting cytokine production, and regulating cell fate, TWEAK/Fn14 activation plays a pivotal role in the pathogenesis of various skin disorders, such as psoriasis, atopic dermatitis, cutaneous vasculitis, human papillomavirus infection and related skin tumors, and cutaneous autoimmune diseases. Therefore, the TWEAK/Fn14 pathway may be a potential target for the development of novel therapeutics for skin inflammatory diseases.http://dx.doi.org/10.1155/2017/6746870 |
| spellingShingle | Qilu Liu Shengxiang Xiao Yumin Xia TWEAK/Fn14 Activation Participates in Skin Inflammation Mediators of Inflammation |
| title | TWEAK/Fn14 Activation Participates in Skin Inflammation |
| title_full | TWEAK/Fn14 Activation Participates in Skin Inflammation |
| title_fullStr | TWEAK/Fn14 Activation Participates in Skin Inflammation |
| title_full_unstemmed | TWEAK/Fn14 Activation Participates in Skin Inflammation |
| title_short | TWEAK/Fn14 Activation Participates in Skin Inflammation |
| title_sort | tweak fn14 activation participates in skin inflammation |
| url | http://dx.doi.org/10.1155/2017/6746870 |
| work_keys_str_mv | AT qiluliu tweakfn14activationparticipatesinskininflammation AT shengxiangxiao tweakfn14activationparticipatesinskininflammation AT yuminxia tweakfn14activationparticipatesinskininflammation |