免疫耐受性. 免疫耐受性. 第三组先天性淋巴细胞通过肠道中介来选择共生细菌特异性的CD4+ T细胞
Matthew R Hepworth1, Thomas C Fung2, Samuel H Masur3
1Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Gastroenterology Division, and Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, NY, USA.
概括
第三组先天性淋巴细胞 (ILC3s) 控制T细胞对肠道细菌的反应. 减少IBD患者ILC3s上的MHCII表明一种新的疾病机制,涉及肠道T细胞选择.
科学领域:
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
- 微生物学 微生物学
背景情况:
- 炎症性CD4 (((+) T细胞反应驱动自身免疫和炎症性肠病 (IBD).
- 胸膜选择限制了自我反应的T细胞,但控制共生细菌特异性T细胞选择的机制尚不清楚.
- 天生的淋巴细胞 (ILC) 对于肠道平衡至关重要.
研究的目的:
- 研究3组先天性淋巴细胞 (ILC3s) 在调节共生细菌特异性T细胞中的作用.
- 为了确定ILC3-内在主要基因相容性复合体II类 (MHCII) 表达是否影响T细胞选择.
- 为了检查儿科IBD患者的结肠ILC3s上的MHCII表达.
主要方法:
- 对ILC3内在MHCII表达调节的分析.
- 评估MHCII(+) ILC3s在激活的共生细菌特异性T细胞中诱导细胞死亡的能力.
- 从儿科IBD患者和健康对照对结肠ILC3s的MHCII表达量的量化.
主要成果:
- ILC3内在的MHCII表达受到类似于胸膜上皮细胞的调节.
- 表达MHCII的ILC3直接诱导激活的开始性细菌特异性T细胞的亡.
- 在儿科IBD患者的结肠ILC3上观察到MHCII表达的减少.
结论:
- 定义了肠道中开始性细菌特异性CD4 ((+) T细胞的新选择途径,由ILC3s介导.
- 这种以ILC3为媒介的T细胞选择过程的失调可能有助于人类IBD的发病.
- 准ILC3功能代表了IBD的潜在治疗策略.
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