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HIV-TB 共感染中抗原呈递缺陷导致 PD1 和 IL-10 的上调。

Defective Antigen Presentation Leads to Upregulation of PD1 and IL-10 in HIV-TB Co-Infection.

机构信息

LEPRA India, BPHRC, Cherlapally, Hyderabad, Andhra Pradesh, India.

Pathology, Microbiology and Immunology Department, Vanderbilt Vaccine Center, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

出版信息

J Interferon Cytokine Res. 2020 Jun;40(6):310-319. doi: 10.1089/jir.2019.0243. Epub 2020 May 22.

Abstract

Human immunodeficiency virus-tuberculosis (HIV-TB) co-infection poses a challenge to the immunologists in developing new diagnostic and therapeutic tools. Mechanisms behind the breakdown of the immune defense of the co-infected individual are poorly known. Numerous studies in HIV alone have revealed the role of PD1, TAP, and IL-10, but not in co-infection. The interaction of the 2 distinct bugs, which is resulting in domination over the host immune system, is still a lacuna. Hence, we aimed to portray functions of IL-10, TAP, and PD1 molecules in HIV-TB co-infection. Co-culture cells challenged with γ-irradiated under various conditions resulted in high interleukin (IL)-10 secretion and high percentage of PD1 expression on CD8 T cells, which might be due to defective antigen presentation of TAP on dendritic cells and macrophages. Herein our observations provide an insight into the escape mechanisms by in HIV-infected individuals from the host immune responses leading to TB co-infection.

摘要

人类免疫缺陷病毒-结核病(HIV-TB)合并感染给免疫学家开发新的诊断和治疗工具带来了挑战。合并感染个体的免疫防御崩溃的机制知之甚少。单独的 HIV 有大量研究揭示了 PD1、TAP 和 IL-10 的作用,但在合并感染中没有。这两种不同的细菌相互作用,导致宿主免疫系统被主导,这仍然是一个空白。因此,我们旨在描述 IL-10、TAP 和 PD1 分子在 HIV-TB 合并感染中的功能。在各种条件下用γ射线辐照共培养细胞会导致白细胞介素(IL)-10 大量分泌和 CD8 T 细胞上 PD1 表达的高百分比,这可能是由于树突状细胞和巨噬细胞上 TAP 的抗原呈递缺陷所致。在此,我们的观察结果提供了对 HIV 感染个体中 逃避宿主免疫反应导致 TB 合并感染的机制的深入了解。

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