AMD3100可预防紫外线诱导的皮肤癌。
AMD3100 protects from UV-induced skin cancer.
作者信息
Byrne Scott N, Sarchio Seri Ne
机构信息
Cellular Photoimmunology Group; Discipline of Infectious Diseases and Immunology; Sydney Medical School; University of Sydney; Sydney, NSW Australia ; Department of Dermatology; Royal Prince Alfred Hospital; Camperdown, NSW Australia ; Discipline of Dermatology at The Bosch Institute; Sydney Medical School; University of Sydney; Sydney, NSW Australia.
Cellular Photoimmunology Group; Discipline of Infectious Diseases and Immunology; Sydney Medical School; University of Sydney; Sydney, NSW Australia ; Department of Dermatology; Royal Prince Alfred Hospital; Camperdown, NSW Australia ; Discipline of Dermatology at The Bosch Institute; Sydney Medical School; University of Sydney; Sydney, NSW Australia ; Faculty of Medicine and Health Sciences; Universiti Putra Malaysia; Malaysia.
出版信息
Oncoimmunology. 2014 Jan 1;3(1):e27562. doi: 10.4161/onci.27562. Epub 2014 Jan 3.
Sunlight causes skin cancer by directly damaging DNA as well as by suppressing antitumor immune responses. A major mechanism whereby sunlight exerts immunosuppressive effects is by modulating the migration of chemokine (C-X-C motif) receptor 4 (CXCR4)-expressing dermal mast cells into and away from the skin. We have demonstrated the importance of this by showing that the systemic administration of the CXCR4 antagonist AMD3100 prevents sunlight-induced immunosuppression as well as the consequent carcinogenic response. Our results highlight the therapeutic potential of antagonizing CXCR4 signaling, especially in individuals who are at high risk of developing skin cancer.
阳光通过直接损伤DNA以及抑制抗肿瘤免疫反应导致皮肤癌。阳光发挥免疫抑制作用的一个主要机制是调节表达趋化因子（C-X-C基序）受体4（CXCR4）的真皮肥大细胞进出皮肤的迁移。我们通过表明全身给予CXCR4拮抗剂AMD3100可预防阳光诱导的免疫抑制以及随之而来的致癌反应，证明了这一点的重要性。我们的结果突出了拮抗CXCR4信号传导的治疗潜力，尤其是在患皮肤癌风险高的个体中。
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