Department of Dermatology, Bispebjerg Hospital, DK-1014 Copenhagen, Denmark.
Biotech Research and Innovation Centre, University of Copenhagen, DK-1014 Copenhagen, Denmark.
Cells. 2020 Nov 10;9(11):2452. doi: 10.3390/cells9112452.
DNA-damaging cancer therapies induce interferon expression and stimulate the immune system, promoting therapy responses. The immune-activating STING (Stimulator of Interferon Genes) pathway is induced when DNA or double-stranded RNA (dsRNA) is detected in the cell cytoplasm, which can be caused by viral infection or by DNA damage following chemo- or radiotherapy. Here, we investigated the responses of cutaneous T-cell lymphoma (CTCL) cells to the clinically applied DNA crosslinking photochemotherapy (combination of 8-methoxypsoralen and UVA light; 8-MOP + UVA). We showed that this treatment evokes interferon expression and that the type III interferon IFNL1 is the major cytokine induced. IFNL1 upregulation is dependent on STING and on the cytoplasmic DNA sensor cyclic GMP-AMP synthase (cGAS). Furthermore, 8-MOP + UVA treatment induced the expression of genes in pathways involved in response to the tumor necrosis factor, innate immune system and acute inflammatory response. Notably, a subset of these genes was under control of the STING-IFNL1 pathway. In conclusion, our data connected DNA damage with immune system activation via the STING pathway and contributed to a better understanding of the effectiveness of photochemotherapy.
DNA 损伤癌症疗法诱导干扰素表达并刺激免疫系统,促进治疗反应。当细胞质中检测到 DNA 或双链 RNA(dsRNA)时,会激活免疫激活 STING(干扰素基因刺激物)途径,这可能是由病毒感染或化疗或放疗后 DNA 损伤引起的。在这里,我们研究了皮肤 T 细胞淋巴瘤(CTCL)细胞对临床应用的 DNA 交联光化学疗法(8-甲氧基补骨脂素和 UVA 光的组合;8-MOP + UVA)的反应。我们表明,这种治疗会引发干扰素表达,并且 III 型干扰素 IFNL1 是主要诱导的细胞因子。IFNL1 的上调依赖于 STING 和细胞质 DNA 传感器环鸟苷酸-腺苷酸合酶(cGAS)。此外,8-MOP + UVA 处理诱导了参与肿瘤坏死因子、先天免疫系统和急性炎症反应的途径中基因的表达。值得注意的是,这些基因的一部分受 STING-IFNL1 途径的控制。总之,我们的数据通过 STING 途径将 DNA 损伤与免疫系统激活联系起来,有助于更好地理解光化学疗法的有效性。