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Dectin-1 非依赖性巨噬细胞吞噬作用

Dectin-1-Independent Macrophage Phagocytosis of .

机构信息

Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A550, Denver, CO 80206, USA.

出版信息

Int J Mol Sci. 2023 Jul 4;24(13):11062. doi: 10.3390/ijms241311062.

DOI:10.3390/ijms241311062
PMID:37446240
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10341562/
Abstract

, a species of nontuberculous mycobacteria (NTM), is an opportunistic pathogen that is readily cleared by healthy lungs but can cause pulmonary infections in people with chronic airway diseases. Although knowledge pertaining to molecular mechanisms of host defense against NTM is increasing, macrophage receptors that recognize remain poorly defined. Dectin-1, a C-type lectin receptor identified as a fungal receptor, has been shown to be a pathogen recognition receptor (PRR) for both and NTM. To better understand the role of Dectin-1 in host defense against , we tested whether blocking Dectin-1 impaired the uptake of by human macrophages, and we compared pulmonary infection in Dectin-1-deficient and wild-type mice. Blocking antibody for Dectin-1 did not reduce macrophage phagocytosis of , but did reduce the ingestion of the fungal antigen zymosan. Laminarin, a glucan that blocks Dectin-1 and other PRRs, caused decreased phagocytosis of both and zymosan. Dectin-1-/- mice exhibited no defects in the control of infection, and no differences were detected in immune cell populations between wild type and Dectin-1-/- mice. These data demonstrate that murine defense against pulmonary infection, as well as ingestion of by human macrophages, can occur independent of Dectin-1. Thus, additional PRR(s) recognized by laminarin participate in macrophage phagocytosis of

摘要

, 一种非结核分枝杆菌(NTM),是一种机会性病原体,在健康的肺部中很容易被清除,但在患有慢性气道疾病的人群中会引起肺部感染。尽管人们对宿主防御非结核分枝杆菌的分子机制的了解在不断增加,但识别的巨噬细胞受体仍未得到明确界定。Dectin-1 是一种已被鉴定为真菌受体的 C 型凝集素受体,已被证明是 和 NTM 的病原体识别受体(PRR)。为了更好地了解 Dectin-1 在宿主防御中的作用,我们测试了阻断 Dectin-1 是否会损害人类巨噬细胞对 的摄取,我们比较了 Dectin-1 缺陷型和野生型小鼠的 肺部感染。Dectin-1 的阻断抗体不会减少巨噬细胞对 的吞噬作用,但会减少真菌抗原几丁质的摄取。几丁质聚糖,一种阻断 Dectin-1 和其他 PRR 的葡聚糖,导致 和几丁质的摄取均减少。Dectin-1-/- 小鼠在控制 感染方面没有缺陷,并且在野生型和 Dectin-1-/- 小鼠之间未检测到免疫细胞群的差异。这些数据表明,鼠类对 肺部感染的防御,以及人类巨噬细胞对 的摄取,可以不依赖于 Dectin-1 发生。因此,被几丁质聚糖识别的其他 PRR(s)参与了巨噬细胞对 的吞噬作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/8ce5a4ee695d/ijms-24-11062-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/a4131486487b/ijms-24-11062-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/8d21b01f8c8a/ijms-24-11062-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/fd93d5315d0c/ijms-24-11062-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/8ce5a4ee695d/ijms-24-11062-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/a4131486487b/ijms-24-11062-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/8d21b01f8c8a/ijms-24-11062-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/fd93d5315d0c/ijms-24-11062-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62b9/10341562/8ce5a4ee695d/ijms-24-11062-g004.jpg

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