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Fcγ受体介导的胞啃作用在系统性自身免疫病易感性中的潜在影响。

Possible implication of Fc γ receptor-mediated trogocytosis in susceptibility to systemic autoimmune disease.

作者信息

Masuda Sakiko, Iwasaki Sari, Tomaru Utano, Baba Tomohisa, Katsumata Kazuaki, Ishizu Akihiro

机构信息

Graduate School of Health Sciences, Hokkaido University, Sapporo 060-0812, Japan.

出版信息

Clin Dev Immunol. 2013;2013:345745. doi: 10.1155/2013/345745. Epub 2013 Sep 4.

DOI:10.1155/2013/345745
PMID:24093044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3777198/
Abstract

Leukocytes can "gnaw away" the plasma membrane of other cells. This phenomenon, called trogocytosis, occurs subsequent to cell-to-cell adhesion. Currently, two mechanisms of trogocytosis, adhesion molecule-mediated trogocytosis and Fc γ receptor-(Fc γ R-) mediated trogocytosis, have been identified. In our earlier study, we established an in vitro model of Fc γ R-mediated trogocytosis, namely, CD8 translocation model from T cells to neutrophils. By using this model, we demonstrated that the molecules transferred to neutrophils via Fc γ R-mediated trogocytosis were taken into the cytoplasm immediately. This result suggests that the chance of molecules transferred via Fc γ R-mediated trogocytosis to play a role on the cell surface could be time-limited. Thus, we consider the physiological role of Fc γ R-mediated trogocytosis as a means to remove antibodies (Abs) that bind with self-molecules rather than to extract molecules from other cells. This concept means that Fc γ R-mediated trogocytosis can be a defense mechanism to Ab-mediated autoimmune response. Moreover, the activity of Fc γ R-mediated trogocytosis was revealed to be parallel to the endocytotic activity of neutrophils, which was critically related to the susceptibility to systemic autoimmune diseases. The collective findings suggest that Fc γ R-mediated trogocytosis could physiologically play a role in removal of Abs bound to self-antigens and prevent autoimmune diseases.

摘要

白细胞能够“侵蚀”其他细胞的质膜。这种现象被称为咬尾吞噬作用,发生在细胞间黏附之后。目前,已经确定了咬尾吞噬作用的两种机制,即黏附分子介导的咬尾吞噬作用和Fcγ受体(FcγR)介导的咬尾吞噬作用。在我们早期的研究中,我们建立了一种FcγR介导的咬尾吞噬作用的体外模型,即CD8从T细胞向中性粒细胞的转位模型。通过使用该模型,我们证明了通过FcγR介导的咬尾吞噬作用转移到中性粒细胞的分子会立即被摄入细胞质中。这一结果表明,通过FcγR介导的咬尾吞噬作用转移的分子在细胞表面发挥作用的机会可能是有时限的。因此,我们认为FcγR介导的咬尾吞噬作用的生理作用是一种清除与自身分子结合的抗体(Abs)的方式,而不是从其他细胞中提取分子。这一概念意味着FcγR介导的咬尾吞噬作用可能是一种针对抗体介导的自身免疫反应的防御机制。此外,FcγR介导的咬尾吞噬作用的活性被发现与中性粒细胞的内吞活性平行,而中性粒细胞的内吞活性与系统性自身免疫疾病的易感性密切相关。这些共同的发现表明,FcγR介导的咬尾吞噬作用在生理上可能在清除与自身抗原结合的抗体以及预防自身免疫疾病方面发挥作用。

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Blood. 2013 Oct 24;122(17):3020-9. doi: 10.1182/blood-2012-12-473744. Epub 2013 Jul 2.
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A rheumatoid factor paradox: inhibition of rituximab effector function.
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Int J Mol Sci. 2021 Feb 24;22(5):2236. doi: 10.3390/ijms22052236.
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Membrane Transfer from Mononuclear Cells to Polymorphonuclear Neutrophils Transduces Cell Survival and Activation Signals in the Recipient Cells via Anti-Extrinsic Apoptotic and MAP Kinase Signaling Pathways.从单核细胞到多形核中性粒细胞的膜转移通过抗外源性凋亡和丝裂原活化蛋白激酶信号通路在受体细胞中转导细胞存活和激活信号。
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