Immune system alterations in amyotrophic lateral sclerosis

肌萎缩侧索硬化 免疫系统 小胶质细胞 神经退行性变 机制(生物学) 神经科学 发病机制 补体系统 神经炎症 疾病 生物 C9orf72 多发性硬化 免疫学 医学 炎症 病理 痴呆 失智症 哲学 认识论
作者
H. Hovden,Jette Lautrup Frederiksen,Stephen Wørlich Pedersen
出处
期刊:Acta Neurologica Scandinavica [Wiley]
卷期号:: n/a-n/a 被引量:30
标识
DOI:10.1111/ane.12125
摘要

Amyotrophic lateral sclerosis is a disease of which the underlying cause and pathogenesis are unknown. Cumulatative data clearly indicates an active participation by the immune system in the disease. An increasingly recognized theory suggests a non-cell autonomous mechanism, meaning that multiple cells working together are necessary for the pathogenesis of the disease. Observed immune system alterations could indicate an active participation in this mechanism. Damaged motor neurons are able to activate microglia, astrocytes and the complement system, which further can influence each other and contribute to neurodegeneration. Infiltrating peripheral immune cells appears to correlate with disease progression, but their significance and composition is unclear. The deleterious effects of this collaborating system of cells appear to outweigh the protective aspects, and revealing this interplay might give more insight into the disease. Markers from the classical complement pathway are elevated where its initiator C1q appears to derive primarily from motor neurons. Activated microglia and astrocytes are found in close proximity to dying motor neurons. Their activation status and proliferation seemingly increases with disease progression. Infiltrating monocytes, macrophages and T cells are associated with these areas, although with mixed reports regarding T cell composition. This literature review will provide evidence supporting the immune system as an important part of ALS disease mechanism and present a hypothesis to direct the way for further studies.

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