Overview of the IL-1 family in innate inflammation and acquired immunity.
Overview of the IL-1 family in innate inflammation and acquired immunity.
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DOI：
10.1111/imr.12621
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发表时间：
2018-01
影响因子：
8.7
通讯作者：
Dinarello CA
中科院分区：
文献类型：
--
作者：
Dinarello CA
细胞因子和受体的白细胞介素-1（IL-1）家族在免疫学中是独特的，因为IL-1家族和Toll样受体（TLR）家族具有相似的功能。比任何其他细胞因子家族，IL-1家族主要与先天免疫相关。超过95%的生物体使用先天免疫机制生存，而不到5%依赖于T细胞和B细胞功能。先天免疫表现为炎症，其可以作为宿主防御机制发挥作用，但当不受控制时对生存有害。IL-1受体和TLR家族的每个成员都含有细胞质Toll-IL-1-受体（TIR）结构域。50个氨基酸的TIR结构域与果蝇中的Toll蛋白高度同源。TIR结构域几乎相同，并且存在于每个TLR和每个IL-1受体家族中。尽管IL-1家族细胞因子成员通过IL-1家族受体触发先天性炎症，但TLR通过细菌、微生物产物、病毒、核酸和损伤相关分子模式（DAMP）触发炎症。事实上，IL-1家族成员IL-1a和IL-33也起DAMP的作用。虽然IL-1家族的炎症特性在先天免疫中占主导地位，但IL-1家族成员可在获得性免疫中发挥作用。本综述是对IL-1家族细胞因子和受体的浓缩更新。
The interleukin-1 (IL-1) family of cytokines and receptors is unique in immunology because the IL-1 family and Toll-like receptor (TLR) families share similar functions. More than any other cytokine family, the IL-1 family is primarily associated with innate immunity. More than 95% of living organisms use innate immune mechanisms for survival whereas less than 5% depend on T-and B-cell functions. Innate immunity is manifested by inflammation, which can function as a mechanism of host defense but when uncontrolled is detrimental to survival. Each member of the IL-1 receptor and TLR family contains the cytoplasmic Toll-IL-1-Receptor (TIR) domain. The 50 amino acid TIR domains are highly homologous with the Toll protein in Drosophila. The TIR domain is nearly the same and present in each TLR and each IL-1 receptor family. Whereas IL-1 family cytokine members trigger innate inflammation via IL-1 family of receptors, TLRs trigger inflammation via bacteria, microbial products, viruses, nucleic acids, and damage-associated molecular patterns (DAMPs). In fact, IL-1 family member IL-1a and IL-33 also function as DAMPs. Although the inflammatory properties of the IL-1 family dominate in innate immunity, IL-1 family member can play a role in acquired immunity. This overview is a condensed update of the IL-1 family of cytokines and receptors.
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影响因子：
16.6
作者：
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通讯作者：
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DOI：
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发表时间：
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发表时间：
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影响因子：
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影响因子：
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