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IL-10调节杆细胞中模式识别受体的表达和激活

Roberto Riquelme-Neira^1,2, Romina Walker-Vergara¹, Joan Antoni Fernández-Blanco²

¹Núcleo de Investigaciones Aplicadas en Ciencias Veterinarias y Agronómicas, Facultad de Medicina Veterinaria y Agronomía, Universidad de Las Américas, Sede Concepción, Chacabuco 539, Concepción 4070254, Chile.

International journal of molecular sciences

|June 28, 2023

概括

互白素-10 (IL-10) 影响杆细胞对微生物触发物的反应. 缺少IL-10会改变模式识别受体 (PRR) 表达和细胞因子的释放,影响免疫细胞的激活.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
微生物学微生物学

背景情况:

乳腺细胞 (MCs) 在对病原体和各种疾病的免疫反应中至关重要.
模式识别受体 (PRRs) 使MC能够检测微生物并启动分泌反应.
互白素-10 (IL-10) 在PRR介导的MC激活中的确切作用仍然不完全理解.

研究的目的:

研究IL-10缺乏对不同巨细胞子集中特定PRRs (TLR2,TLR4,TLR7,NOD2) 的激活的影响.
分析IL-10如何影响瘤细胞中PRRs的表达和随后的细胞因子分泌 (IL-6,TNFα).
为了确定IL-10对巨细胞对PRR刺激的反应的年龄相关影响.

主要方法:

在粘膜状MCs (MLMCs) 和腹膜衍生培养MCs (PCMCs) 中对托尔类受体2 (TLR2),TLR4,TLR7和核酸结合寡合化域含蛋白2 (NOD2) 的激活进行分析.
在不同年龄 (6周和20周) 的IL-10淘汰赛 (IL-10-/-) 和野生型 (WT) 小鼠之间比较PRR表达和细胞因子分泌.
测量IL-6和瘤坏死因子α (TNFα) 的分泌,以特定的PRR配体进行刺激后.

主要成果:

IL-10-/-小鼠在6周后在MLMC中表现出TLR4和NOD2的减少表达,并在20周后表现出TLR7.
与WT相比,TLR2激活导致IL-10-/- MCs中的IL-6和TNFα分泌量减少.
NOD2连接体没有诱导细胞因子的释放,老年IL-10-/- MCs中TLR2/TLR4反应减少.

结论:

巨细胞中的PRR激活是一个复杂的过程,受细胞表型,特定的激活配体,动物年龄和IL-10存在的影响.
IL-10在调节巨细胞对各种PRR的反应中发挥着重要作用,影响细胞因子的产生.
这些发现突显了巨细胞免疫的复杂调节,并表明了与IL-10相关的免疫失调的潜在治疗点.

关键词:

货币市场中心MMC 在NOD2中,NOD2是NOD2.这是PCMCMC的PCMC.这就是PRRR.这是一个TLR.介质蛋白-10 介质蛋白-10 的作用.

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