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针对包含在猴病毒40病毒样颗粒中的抗原内细胞毒性T淋巴细胞表位产生的γ干扰素。

Interferon-γ production in response to the cytotoxic T lymphocyte epitope within an antigen incorporated in simian virus 40 virus-like particles.

作者信息

Watanabe Takeharu, Hayashi Masayuki, Arai Masaaki, Matsushita Sho, Handa Hiroshi, Kawano Masaaki

机构信息

Vaccine Sohyaku Group Modality Laboratories Sohyaku. Innovation Research Division Mitsubishi Tanabe Pharma Corporation, 1000 Kamoshida, Aoba-ku, Yokohama, 227-0033, Japan.

Department of Allergy and Immunology, Faculty of Medicine, Saitama Medical University, 38 Morohongo, Moroyama, Saitama, 350-0495, Japan.

出版信息

Heliyon. 2025 Jan 10;11(2):e41729. doi: 10.1016/j.heliyon.2025.e41729. eCollection 2025 Jan 30.

DOI:10.1016/j.heliyon.2025.e41729
PMID:39897799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11786666/
Abstract

In a previous study, we showed that administration of antigen-incorporated virus-like particles (VLPs) derived from simian virus 40 (SV40) induces production of cytotoxic T lymphocytes (CTL), as well as antibodies against the incorporated antigen(s), without the need for an adjuvant; however, it remains unclear how immune cells recognize and respond to the SV40 capsid because SV40 VLPs did not upregulate expression of maturation markers on dendritic cells. In this study, administration of chicken ovalbumin (OVA) incorporated within SV40 VLPs induced interferon (IFN)-γ production in response to the OVA CTL epitope. IFN-γ production in response to the OVA CTL epitope was not inhibited in B cell-depleted mice, but it was inhibited in cluster of differentiation (CD)4 T cell-depleted mice. Administration of SV40 VLPs upregulated expression of CD63/CD68/CD83/CD86/CD196, and induced secretion of C-C chemokine ligand (CCL)3 and CCL4, by B cells, as well as secretion of CCL4 by T cells and tumor necrosis factor-α by bone marrow-derived dendritic cells.

摘要

在先前的一项研究中,我们发现,给予源自猿猴病毒40(SV40)的掺入抗原的病毒样颗粒(VLP)可诱导细胞毒性T淋巴细胞(CTL)的产生以及针对掺入抗原的抗体的产生,而无需佐剂;然而,目前尚不清楚免疫细胞如何识别和应答SV40衣壳,因为SV40 VLP并未上调树突状细胞上成熟标志物的表达。在本研究中,给予掺入SV40 VLP内的鸡卵清蛋白(OVA)可诱导针对OVA CTL表位产生干扰素(IFN)-γ。在B细胞缺失的小鼠中,针对OVA CTL表位产生的IFN-γ未受抑制,但在分化簇(CD)4 T细胞缺失的小鼠中受到抑制。给予SV40 VLP可上调B细胞的CD63/CD68/CD83/CD86/CD196的表达,并诱导B细胞分泌C-C趋化因子配体(CCL)3和CCL4,以及诱导T细胞分泌CCL4和骨髓来源的树突状细胞分泌肿瘤坏死因子-α。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/b1810d32b182/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/ad74ce0f8ae9/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/84b2b90662d2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/ae7c407dde4d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/cc3c655d3748/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/92c513fcf10b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/b1810d32b182/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/ad74ce0f8ae9/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/84b2b90662d2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/ae7c407dde4d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/cc3c655d3748/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/92c513fcf10b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba8/11786666/b1810d32b182/gr5.jpg

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