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人针对. 的抗体反应的功能。

Functionality of the human antibody response to .

机构信息

Institute of Biochemistry and Biophysics, Faculty of Biological Sciences, Friedrich Schiller University, Jena, Germany.

Leibniz Institute for Natural Product Research and Infection Biology, Hans Knöll Institute, Jena, Germany.

出版信息

Virulence. 2021 Dec;12(1):3137-3148. doi: 10.1080/21505594.2021.2015116.

DOI:10.1080/21505594.2021.2015116
PMID:34923920
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8923069/
Abstract

is a common commensal on human mucosal surfaces, but can become pathogenic, e.g. if the host is immunocompromised. While neutrophils, macrophages and T cells are regarded as major players in the defense against pathogenic , the role of B cells and the protective function of their antibodies are less well characterized. In this study, we show that human serum antibodies are able to enhance the association of human THP-1 monocyte-like cells with cells. Human serum antibodies are also capable of inhibiting the adherence and damage dealt to epithelial cells. Furthermore, human serum antibodies impair invasion of human oral epithelial cells by blocking induced endocytosis and consequently host cell damage. While aspartic proteases secreted by are able to cleave human IgG, this process does not appear to affect the protective function of human antibodies. Thus, humans are equipped with a robust antibody response to , which can enhance antifungal activities and prevent fungal-mediated epithelial damage.

摘要

是人类黏膜表面的常见共生菌,但也可能成为病原体,例如当宿主免疫功能低下时。尽管中性粒细胞、巨噬细胞和 T 细胞被认为是抵御病原体的主要参与者,但 B 细胞的作用及其抗体的保护功能尚未得到充分描述。在这项研究中,我们表明人血清抗体能够增强人类 THP-1 单核细胞样细胞与 细胞的结合。人血清抗体也能够抑制黏附并减轻对上皮细胞的损伤。此外,人血清抗体通过阻断诱导的内吞作用从而阻止宿主细胞损伤来抑制 的侵袭。尽管 分泌的天冬氨酸蛋白酶能够切割人 IgG,但该过程似乎并不影响人抗体的保护功能。因此,人类对 具有强大的抗体反应,这可以增强抗真菌活性并防止真菌介导的上皮损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/8ce579cf3ae9/KVIR_A_2015116_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/f6bca4f27da8/KVIR_A_2015116_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/dfae82e4f4b7/KVIR_A_2015116_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/3d10feede96f/KVIR_A_2015116_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/6d622d859201/KVIR_A_2015116_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/8ce579cf3ae9/KVIR_A_2015116_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/f6bca4f27da8/KVIR_A_2015116_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/dfae82e4f4b7/KVIR_A_2015116_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/3d10feede96f/KVIR_A_2015116_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/6d622d859201/KVIR_A_2015116_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/877e/8923069/8ce579cf3ae9/KVIR_A_2015116_F0005_B.jpg

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