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通过促进树突细胞依赖性炎症,CXCR1驱动EAE和ARDS的致病性

Wei Zhuang^1,2,3, Jinfeng Zhou¹, Lan Zhong⁴

¹Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200092, China.

Cell death & disease

|September 14, 2023

概括

化基因受体CXCR1驱动了诸如多发性硬化症和急性呼吸困扰综合征等自身免疫性疾病的炎症. 向树突细胞 (DCs) 中的CXCR1可以降低疾病的严重程度和炎症因子的产生.

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:

树突细胞 (DCs) 通过化学受体分泌化学,通过化学受体调节炎症和自身免疫.
化基因受体CXCR1在实验性自身免疫脑膜炎 (EAE) 和急性呼吸困扰综合征 (ARDS) 中的特定作用尚不清楚.

研究的目的:

研究CXCR1在EAE和ARDS中的作用.
探索CXCR1作为潜在的炎症和自身免疫性疾病的治疗点.

主要方法:

在多发性硬化症 (MS) 患者中评估CXCR1水平.
使用CXCR1淘汰和DC特定的淘汰小鼠模型用于EAE.
在使用脂聚糖 (LPS) 的小鼠中诱导ARDS.
测量了炎症因素 (IL-6,IL-12p70) 和疾病严重程度.

主要成果:

与健康对照人群相比,MS患者的CXCR1水平升高.
淘汰CXCR1改善了EAE的严重程度,并抑制了IL-6/IL-12p70的产生.
特定于DC的CXCR1删除和CXCL5中和减少了EAE.
确定了一种积极的反循环,涉及CXCL5/CXCR1/HIF-1α调节DC中的IL-6/IL-12p70.
在DC中CXCR1缺陷降低了IL-6/IL-12p70的产生和LPS诱导的ARDS中的肺损伤.

结论:

CXCR1在控制DC介导的炎症和自身免疫性疾病方面发挥着关键作用.
CXCR1是MS和ARDS等疾病的潜在治疗标.

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