免疫和非免疫炎症细胞参与自身免疫纤维化:新发现
Margherita Sisto1, Sabrina Lisi1
1Department of Translational Biomedicine and Neuroscience (DiBraiN), Section of Human Anatomy and Histology, University of Bari "Aldo Moro", 70124 Bari, Italy.
Journal of clinical medicine
|June 10, 2023
概括
纤维化是一个重要的健康问题,它是由涉及免疫和非免疫细胞的未知机制引起的. 本综述探讨了驱动纤维化疾病,特别是自身免疫性疾病的沟通通路径.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 病理学 病理学 病理学
背景情况:
- 纤维化是一个主要的健康问题,对病原体激活的了解很少.
- 它经常是慢性炎症性自身免疫性疾病的次要发展,并以免疫细胞透为标志.
- 免疫和非免疫细胞都通过炎症介质的产生促进纤维化.
研究的目的:
- 审查有关纤维化开始和延续机制的最新发现.
- 为了阐明在纤维性疾病中免疫和非免疫细胞之间的异常通信.
- 了解非免疫细胞在炎症性自身免疫性疾病的发病过程中的作用.
主要方法:
- 关于纤维化机制的最新研究的文献综述.
- 在纤维化过程中对细胞相互作用的分析.
- 探索细胞因子概况和炎症媒介.
主要成果:
- 纤维化组织显示单核免疫细胞透,具有亲炎性和亲纤维化细胞因子概况.
- 非免疫细胞 (上皮细胞,内皮细胞,纤维细胞) 可以产生炎症介质,加剧纤维化.
- 免疫和非免疫细胞之间的异常通信创造了一个恶性循环,推动了纤维细胞的进化.
结论:
- 精确的细胞机制驱动纤维化仍然不完全理解.
- 非免疫细胞免疫调节的缺陷有助于炎症疾病的致病性.
- 了解细胞-细胞通信对于解决自身免疫性疾病中的纤维化进化至关重要.
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