Department of Medicine, Section of Dermatology, University of Chicago, Chicago, IL.
Department of Medicine, Section of Hematology and Oncology, University of Chicago, Chicago, IL.
Photochem Photobiol. 2023 Mar;99(2):850-856. doi: 10.1111/php.13684. Epub 2022 Aug 12.
Excessive, high doses of ultraviolet B (UVB) UVB irradiation are known to cause skin cancer, aging and immunosuppression. On the contrary, moderate low doses of UVB irradiation are shown to be essential and beneficial to human health, including a tumor-suppressive effect. However, the mechanism by which low levels of UVB suppress tumorigenesis remains unclear. Here, using tumor-bearing mouse models, we show that moderate low repetitive UVB irradiation increases the percentage of activated CD4 and CD8 T cells, and CD103 conventional type 1 dendritic cells (cDC1s), while it decreases the number of immunosuppressive, M2-like macrophages in the tumors. Finally, in mice, deletion of Batf3, a transcription factor critical for the development of conventional dendritic cells, including the CD103 cDC1s, showed increased tumor growth in both sham- and UVB-irradiated mice. Our findings demonstrate that moderate low UVB irradiation inhibits M2-like tumor-associated macrophages, increases CD103 cDC1s and promotes antitumor immunity in mice with an established tumor.
过量、高强度的紫外线 B(UVB)辐射已知会导致皮肤癌、衰老和免疫抑制。相反,适度的低剂量 UVB 辐射对人类健康是必不可少且有益的,包括抑制肿瘤的作用。然而,低水平 UVB 抑制肿瘤发生的机制尚不清楚。在这里,我们使用荷瘤小鼠模型表明,适度低重复 UVB 辐射会增加激活的 CD4 和 CD8 T 细胞以及 CD103 传统型 1 树突状细胞(cDC1)的百分比,同时减少肿瘤中免疫抑制的 M2 样巨噬细胞数量。最后,在小鼠中,缺失转录因子 Batf3(其对包括 CD103 cDC1 在内的传统树突状细胞的发育至关重要),在 sham 和 UVB 照射的小鼠中均显示出肿瘤生长增加。我们的研究结果表明,适度低剂量的 UVB 辐射可抑制 M2 样肿瘤相关巨噬细胞,增加 CD103 cDC1 并促进已建立肿瘤小鼠的抗肿瘤免疫。