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Updated: Jul 6, 2025

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通过ICAM-1介导的细胞-细胞粘附在人类B细胞分化和IgG生产方面发挥着双重作用

Shuai Liu1,2,3, Zhi-Cui Liu4, Mei-Yu Zhang1

  • 1Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

iScience
|January 1, 2024
PubMed

Insights

CD4+ T 细胞上增加的细胞间粘附分子1 (ICAM-1) 增强了 T-B 细胞的粘附,但减少了 B 细胞的分化和 IgG 生产,部分是通过 B 细胞的 PD-1 诱导.

科学领域:

  • 免疫学 免疫学 免疫学
  • 细胞生物学 细胞生物学
  • 分子医学是分子医学.

背景情况:

  • 细胞间粘附分子1 (ICAM-1) 对于细胞间粘附和免疫细胞相互作用至关重要.
  • CD4+ T细胞和B细胞在免疫反应中合作,包括B细胞激活和分化.

研究的目的:

  • 研究ICAM-1在CD4+T细胞在T-B细胞相互作用和B细胞分化中的作用.
  • 探索ICAM-1介导粘附对IgG产生的影响,并确定潜在的机制.

主要方法:

  • 纯化的人类CD4+T细胞被用抗CD3/CD28激发.
  • 刺激的CD4+T细胞与B细胞共同培养.
  • 分析ICAM-1和PD-1表达,B细胞分化标志物,IgG产生和信号通路 (ERK1/2,Blimp-1/IRF4).
  • 研究来自系统性红斑狼 (SLE) 患者的CD4+T细胞.

主要成果:

  • 对CD4+T细胞增强的ICAM-1增加了T-B细胞粘附,但降低了B细胞分化和IgG生产.
  • 在与过度激活的CD4+T细胞共同培养后,观察到B细胞上PD-1表达的增加.
  • ICAM-1封锁通过ERK1/2和Blimp-1/IRF4上调促进了IgG的产生.
  • 患有高ICAM-1的SLE患者的CD4+T细胞显示IgG的产生减少.

结论:

  • 通过ICAM-1-介导的CD4+ T-B细胞粘附在B细胞分化和IgG生产中具有双重作用,受B细胞PD-1水平的影响.
  • 对B细胞的PD-1诱导作为B细胞分化的内在检查点.
  • 在SLE中失调的ICAM-1表达可能导致B细胞功能受损.
抽象的

No abstract available in PubMed .

关键词:
癌症 癌症 癌症 癌症细胞生物学 细胞生物学免疫系统的组成部分免疫学 免疫学 免疫学分子生物学分子生物学

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