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MiR-155 负面调节了艾滋病毒感染的进发者的抗病毒本性反应

Puja Pawar¹, Jyotsna Gokavi¹, Shilpa Wakhare¹

¹Division of Immunology and Serology, ICMR-National AIDS Research Institute, Pune 411026, India.

|November 25, 2023

概括

艾滋病毒疾病进展者的功能失调的先天免疫与miR-155有关. 抑制miR-155可以恢复托尔类受体 (TLR) 介导的反应和宿主限制因子,这为抗击艾滋病毒进展提供了潜在的策略.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
分子生物学分子生物学

背景情况:

艾滋病毒感染严重损害宿主免疫力,抗逆转录病毒疗法只能部分恢复免疫功能.
功能失调的先天免疫反应,特别是托尔类受体 (TLR) 介导的途径,在艾滋病毒疾病进展者中了解得很少.
主体和病毒因素影响艾滋病毒疾病进展率.

研究的目的:

研究HIV疾病进展者的功能障碍天生的免疫反应背后的机制.
检查TLRs和先天性细胞因子在HIV感染中的作用.
探索TLR激动剂在恢复进发者的先天性免疫功能方面的潜力.

主要方法:

在艾滋病毒感染者 (进展者和长期非进展者) 和艾滋病毒未感染者中,对TLR和先天细胞因子的基因表达概况.
用TLR3,TLR7和TLR9激动剂刺激周围血液单核细胞 (PBMC).
探索miR-155的作用,通过其抑制从前进者的PBMCs.

主要成果:

进展者表现出失调的TLR介导的先天反应.
使用TLR激动剂 (多:I:C,GS-9620,ODN 2216) 的刺激增加了IFN-α,IFN-β和IL-6的表达.
在进步者中观察到miR-155表达的增加;其抑制上调TLR3,NF-κB,IRF-3,TNF-α和宿主限制基因 (APOBEC-3G,IFITM-3,IFI-16,BST-2).

结论:

miR-155对TLR介导的细胞因子产生和对抗HIV反应至关重要的宿主限制因子进行负面调节.
向miR-155是一个潜在的治疗策略,可以缓解艾滋病毒疾病的进展.

关键词:

艾滋病病毒艾滋病病毒艾滋病病毒长期国家安全计划 (LTNP) 是一个长期国家安全计划.TLRs 是一个 TLR.疾病的进展疾病的进展主机限制因素的主机限制因素这是天生的,天生的.在 miR-155 系统中,它是 miR-155 的.

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