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CD301b乳腺瘤微环境中的莱克表达增加了瘤的生长

Ahmet Ozdilek¹, Amy V Paschall¹, Zahra Nawaz¹

¹Department of Biochemistry, Emory Vaccine Center, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322.

Research square

|December 11, 2025

概括

异常瘤糖化对免疫识别产生影响. 研究人员发现,C型莱克CD301b通过与髓状细胞相互作用,促进乳腺瘤生长,这表明它是治疗点.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
葡萄糖生物学葡萄糖生物学

背景情况:

异常的瘤糖化对免疫识别有影响,但其在瘤进展中通过甘氨酸-莱克相互作用的作用尚不清楚.
瘤微环境 (TME) 在癌症进展和免疫规避中发挥着关键作用.
C型莱克受体是免疫系统中细胞与细胞相互作用的关键媒介.

研究的目的:

为了研究C型莱克受体CD301b (编码为*Mgl2*) 在乳腺瘤微环境中的免疫活动调节中的作用.
为了阐明影响乳腺癌瘤进展的特定的糖甘-莱克相互作用.
确定CD301b作为重编程乳腺癌TME的潜在治疗标.

主要方法:

利用小鼠三阴性乳腺癌模型研究瘤生长和免疫细胞相互作用.
采用CD301b消耗和遗传淘汰策略来评估其功能作用.
进行了表型分析,单细胞RNA测序和瘤的转录基因分析.

主要成果:

表达Tn糖抗原的瘤表现出加速生长,由CD301b表达免疫细胞促进.
CD301b的枯竭或遗传损失显著抑制了瘤的生长,这表明它在髓质瘤相互作用中的作用.
鉴定出CD301b+细胞是2型常规树突细胞 (cDC2s),其人类正义细胞CLEC10A在人类的cDC2类细胞和巨细胞中表达,这表明其功能得到保护.
缺乏*Mgl2*的小鼠表现出具有炎症性,免疫激活表型的瘤,表明抗瘤免疫力增强.

结论:

CD301b 作为乳腺瘤微环境中的免疫活动的关键调节者,促进瘤的进展.
这项研究确立了异常瘤糖化和骨髓状细胞中莱克信号传递之间的直接联系.
CD301b是调节瘤免疫微环境和增强乳腺癌抗瘤免疫力的有前途的治疗标.

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