SCF和IL-33调节小鼠大细胞的表型和功能性可塑性,支持一种促炎性微环境
Rosa Molfetta1, Mario Lecce2,3, Nadia D Milito2
1Department of Molecular Medicine, Laboratory affiliated to Istituto Pasteur Italia - Fondazione Cenci Bolognetti, Sapienza University of Rome, 00161, Rome, Italy. rosa.molfetta@uniroma1.it.
Cell death & disease
|September 20, 2023
概括
结直肠癌中的巨细胞 (MCs) 通过释放IL-6和TNF-α来促进瘤生长. 干细胞因子 (SCF) 和IL-33驱动这种亲瘤源的MC表型,创造了一个亲炎症的瘤微环境.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
背景情况:
- 巨细胞 (MCs) 是在瘤微环境 (TME) 中发现的免疫细胞.
- MCs在癌症中具有双重作用,可能促进或抑制瘤的进展.
- 它们的功能受到MCs对微环境刺激反应的可塑性质的影响.
研究的目的:
- 为了研究巨细胞在结肠炎相关的结肠直肠癌中的作用.
- 鉴定瘤微环境中的巨细胞表型和介质.
- 在这种情况下,确定干细胞因子 (SCF) 和干细胞因子介质素-33 (IL-33) 对巨细胞功能的影响.
主要方法:
- 使用了一种与结肠炎相关的结肠直肠癌的小鼠模型.
- 采用多色流细胞计和共聚焦显微镜来分析乳腺细胞.
- 通过SCF和IL-33刺激的研究的初级巨细胞培养物.
主要成果:
- 与瘤相关的巨细胞表现出结缔组织表型.
- 这些巨细胞释放出高水平的互白素-6 (IL-6) 和瘤坏死因子-α (TNF-α).
- 刺激SCF和IL-33诱导了巨细胞中的促炎性细胞因子的产生.
结论:
- 持续的SCF和IL-33刺激在结肠转化过程中驱动了一种亲瘤性乳腺细胞子集的积累.
- 这些巨细胞分泌IL-6和TNF-α,维持一种促炎性微环境,支持癌症的进展.
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