中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (12): 2691-2692.doi: 10.4103/1673-5374.335808

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

Aicardi-Goutieres综合征和神经炎症小鼠模型中炎症细胞因子的产生

  

  • 出版日期:2022-12-15 发布日期:2022-05-05

Inflammatory cytokine production in a mouse model of Aicardi-Goutieres syndrome and neuroinflammation

Clayton A. Wiley*, Qingde Wang*   

  1. Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA (Wiley CA)
    Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA (Wang Q)
  • Online:2022-12-15 Published:2022-05-05
  • Contact: Qingde Wang, MD, PhD, wangqd@pitt.edu; Clayton A. Wiley, MD, wileyca@upmc.edu.
  • Supported by:
    This study was supported by National Institute of Health, Grant number: R01AI139544.

摘要: https://orcid.org/0000-0002-2482-7972 (Qingde Wang)
https://orcid.org/0000-0002-2697-7691 (Clayton A. Wiley)

Abstract: Most neurological diseases are associated with a tissue injury that is detected by the innate immune response (IIR), leading to an inflammatory component. The IIR is activated through conserved Pattern Recognition Receptors, including membrane bound Toll like receptors (TLRs), intracellular nucleotide-binding oligomerization domain like receptors and the receptors for advanced glycation end-products (Amor et al., 2010; Heppnerrt et al., 2015). These receptors detect highly conserved structural motifs of damaged or stressed tissues (danger-associated molecular patterns (DAMP)). Cytosolic receptors of nucleic acids, such as cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) and melanoma differentiation associated gene 5 (MDA-5) can also trigger IIR activation leading to interferon (IFN) and IFN stimulated gene (ISG) expression through DNA/RNA sensing signaling pathways (Yang and Li, 2020). Once bound to their cognate receptor, the recognition complexes migrate into the nucleus and initiate different signaling cascades that eventually lead to central nervous system (CNS) inflammation.