Vilia Maria Giovanna, Fonte Eleonora, Veliz Rodriguez Tania, Tocchetti Marta, Ranghetti Pamela, Scarfò Lydia, Papakonstantinou Nikos, Ntoufa Stavroula, Stamatopoulos Kostas, Ghia Paolo, Muzio Marta
a Division of Experimental Oncology , IRCCS San Raffaele Scientific Institute , Milano , Italy.
b Vita-Salute San Raffaele University , Milano , Italy.
Leuk Lymphoma. 2017 Oct;58(10):2419-2425. doi: 10.1080/10428194.2017.1295142. Epub 2017 Feb 28.
Toll interleukin-1 receptor 8 (also known as TIR8, SIGIRR, or IL1R8) is a transmembrane receptor that inhibits inflammation. Accordingly, genetic inactivation of this protein exacerbates chronic inflammation and inflammation-associated tumors in mice. In particular, lack of TIR8 triggers leukemia progression in a mouse model of chronic lymphocytic leukemia (CLL), supporting its role as a novel tumor restrainer. The aim of this study was to measure the amount of TIR8 mRNA and protein in CLL cells, and to analyze its regulation of expression. Circulating leukemic cells expressed lower levels of TIR8 compared to normal B-lymphocytes. Treatment of CLL cells with Azacytidine restored higher levels of TIR8 suggesting that DNA methylation may be involved in modulating TIR8 expression, with implications for novel therapeutic strategies.
Toll白细胞介素-1受体8（也称为TIR8、SIGIRR或IL1R8）是一种抑制炎症的跨膜受体。因此，该蛋白的基因失活会加剧小鼠的慢性炎症和炎症相关肿瘤。特别是，在慢性淋巴细胞白血病（CLL）小鼠模型中，TIR8的缺失会引发白血病进展，这支持了其作为新型肿瘤抑制因子的作用。本研究的目的是测量CLL细胞中TIR8 mRNA和蛋白的量，并分析其表达调控。与正常B淋巴细胞相比，循环白血病细胞表达的TIR8水平较低。用阿扎胞苷处理CLL细胞可恢复较高水平的TIR8，这表明DNA甲基化可能参与调节TIR8的表达，这对新型治疗策略具有重要意义。
