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在活体研究中,在瘤生长的背景下,对巨细胞再极化的潜在机制进行了研究

N Fedosova¹, A Chumak¹, N Cheremshenko¹

¹R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology of the NAS of Ukraine, Kyiv, Ukraine.

Experimental oncology

|June 9, 2024

概括

来自B. subtilis的细菌莱克通过保持巨细胞M1极化和增强自然杀手 (NK) 细胞和细胞毒性T淋巴细胞活性来增强小鼠的抗瘤免疫力. 这表明STAT和IRF信号通路在免疫反应调节中的作用.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
在瘤学瘤学.

背景情况:

腹膜巨细胞 (Mph) 在抗瘤免疫中起着至关重要的作用,M1和M2表型表现出不同的功能.
瘤生长可能导致免疫抑制,通常与M2巨细胞两极分化和降低效应细胞活性有关.
细菌莱克正在研究它们在癌症治疗中的免疫调节特性.

研究的目的:

在小鼠模型中,研究B. subtilis IMV B-7724讲素对抗瘤免疫因子的影响.
分析腹Mph M1/M2复极化的机制,在瘤生长过程中由细菌莱克诱导.
评估莱克给药对自然杀手 (NK) 细胞,细胞毒性T淋巴细胞 (CTLs) 和细胞因子概况的影响.

主要方法:

携带埃里希腺癌 (ACE) 的Balb/c小鼠接受了B. subtilis IMV B-7724 莱克 (1 mg/kg,10剂量) 的治疗.
免疫学评估包括Mph,NK细胞和CTLs的功能活性,以及细胞因子 (IFN-γ,IL-4) 水平.
在Mph中评估了STAT-1,STAT-6,IRF5和IRF4的mRNA表达,以了解两极化机制.

主要成果:

莱克的使用保留了腹Mph的M1功能状态,并保持了CD8+T淋巴细胞细胞毒性活性.
观察到NK细胞活性的显著增加 (完整的2.7倍,未经治疗的12.9倍).
在Mph/CD8+T淋巴细胞活性,NO/Arg比率和抗瘤有效性之间发现了积极的相关性,表明通过STAT和IRF通路间接Mph偏振.

结论:

来自B. subtilis的细菌莱克可以在携带ACE的小鼠中将腹膜Mph重新偏向M1表型.
这种再极化不仅涉及直接的莱克受体相互作用,还涉及NK细胞和T淋巴细胞的活性.
STAT和IRF信号通路涉及到由莱克诱导的Mph极化过程,有助于抗瘤免疫力.

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