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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.

bioRxiv : the preprint server for biology

|December 3, 2025

概括

异常瘤糖化对免疫识别产生影响. 这项研究确定CD301b+髓质细胞是乳腺瘤生长的关键驱动因素,表明CD301b是治疗标.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
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) 在癌症进展和免疫逃避中发挥着关键作用.
了解特定的甘氨酸-莱克相互作用对于开发新型癌症疗法至关重要.

研究的目的:

研究C型莱克受体CD301b在乳腺瘤进展中的作用.
为了阐明CD301b+免疫细胞在瘤微环境中的功能.
确定潜在的治疗点,用于重编程乳腺癌TME.

主要方法:

使用了一种小鼠三阴性乳腺癌模型.
采用了CD301b消耗和遗传淘汰策略.
进行了表型分析,单细胞RNA测序和转录基因分析.

主要成果:

表达Tn糖抗原的瘤表现出加速生长,CD301b+免疫细胞的促进.
丢失或耗尽CD301b显著抑制瘤生长,表明CD301b促进瘤进展.
CD301b+细胞被确定为2型常规树突细胞 (cDC2s),它们的人类正体细胞CLEC10A在人类乳腺癌中表达.
缺乏Mgl2 (编码CD301b) 的小鼠表现出转向具有增强抗瘤免疫力的免疫活性状态的转变.

结论:

骨髓状细胞,特别是cDC2s中的CD301b信号促进乳腺瘤的进展.
异常瘤糖化和CD301b介导的髓状细胞相互作用是TME的关键调节者.
CD301b是增强乳腺癌抗瘤免疫力的有前途的治疗标.

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