PB101是一种靶向VEGF和PlGF的诱饵蛋白,可增强抗肿瘤免疫并抑制肿瘤进展和转移。

IF 7.2 2区 医学
Oncoimmunology Pub Date : 2023-09-20 eCollection Date: 2023-01-01 DOI:10.1080/2162402X.2023.2259212
Eun-Jin Go, Hannah Yang, Seung Joon Lee, Hyun Gul Yang, Jin A Shin, Won Suk Lee, Hye Seong Lim, Hong Jae Chon, Chan Kim
{"title":"PB101是一种靶向VEGF和PlGF的诱饵蛋白,可增强抗肿瘤免疫并抑制肿瘤进展和转移。","authors":"Eun-Jin Go,&nbsp;Hannah Yang,&nbsp;Seung Joon Lee,&nbsp;Hyun Gul Yang,&nbsp;Jin A Shin,&nbsp;Won Suk Lee,&nbsp;Hye Seong Lim,&nbsp;Hong Jae Chon,&nbsp;Chan Kim","doi":"10.1080/2162402X.2023.2259212","DOIUrl":null,"url":null,"abstract":"<p><p>Antiangiogenic therapy is a recognized method for countering the immunosuppressive tumor microenvironment (TME) and improving anti-tumor immunity. PB101 is a glycosylated decoy receptor that binds to VEGF-A and PlGF with high affinity, based on the VEGFR1 backbone. Here, we elucidated PB101-induced remodeling of tumor angiogenesis and immunity, which enhances anti-PD-L1 immune checkpoint blockade. PB101 inhibited tumor growth by suppressing angiogenesis and enhancing CD8<sup>+</sup> T cell infiltration into the tumors. PB101 induced robust reprogramming of antitumor immunity and activates intratumoral CD8<sup>+</sup> T cells. Anti-tumor efficacy of PB101 is mostly dependent on CD8<sup>+</sup> T cells and IFN-γ. PB101 reprograms tumor immunity in a manner distinct from that of the conventional VEGF decoy receptor, VEGF-trap. With its potent immune-modulating capability, PB101 synergizes with an anti-PD-L1, triggering strengthened antitumor immunity. Combining PB101 and anti-PD-L1 could establish durable protective immunity against tumor recurrence and metastasis. The findings of this study offer scientific rationales for further clinical development of PB101, particularly when used in combination with immune checkpoint inhibitors, as a potential treatment for advanced cancers.</p>","PeriodicalId":19683,"journal":{"name":"Oncoimmunology","volume":"12 1","pages":"2259212"},"PeriodicalIF":7.2000,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/88/09/KONI_12_2259212.PMC10515676.pdf","citationCount":"0","resultStr":"{\"title\":\"PB101, a VEGF- and PlGF-targeting decoy protein, enhances antitumor immunity and suppresses tumor progression and metastasis.\",\"authors\":\"Eun-Jin Go,&nbsp;Hannah Yang,&nbsp;Seung Joon Lee,&nbsp;Hyun Gul Yang,&nbsp;Jin A Shin,&nbsp;Won Suk Lee,&nbsp;Hye Seong Lim,&nbsp;Hong Jae Chon,&nbsp;Chan Kim\",\"doi\":\"10.1080/2162402X.2023.2259212\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Antiangiogenic therapy is a recognized method for countering the immunosuppressive tumor microenvironment (TME) and improving anti-tumor immunity. PB101 is a glycosylated decoy receptor that binds to VEGF-A and PlGF with high affinity, based on the VEGFR1 backbone. Here, we elucidated PB101-induced remodeling of tumor angiogenesis and immunity, which enhances anti-PD-L1 immune checkpoint blockade. PB101 inhibited tumor growth by suppressing angiogenesis and enhancing CD8<sup>+</sup> T cell infiltration into the tumors. PB101 induced robust reprogramming of antitumor immunity and activates intratumoral CD8<sup>+</sup> T cells. Anti-tumor efficacy of PB101 is mostly dependent on CD8<sup>+</sup> T cells and IFN-γ. PB101 reprograms tumor immunity in a manner distinct from that of the conventional VEGF decoy receptor, VEGF-trap. With its potent immune-modulating capability, PB101 synergizes with an anti-PD-L1, triggering strengthened antitumor immunity. Combining PB101 and anti-PD-L1 could establish durable protective immunity against tumor recurrence and metastasis. The findings of this study offer scientific rationales for further clinical development of PB101, particularly when used in combination with immune checkpoint inhibitors, as a potential treatment for advanced cancers.</p>\",\"PeriodicalId\":19683,\"journal\":{\"name\":\"Oncoimmunology\",\"volume\":\"12 1\",\"pages\":\"2259212\"},\"PeriodicalIF\":7.2000,\"publicationDate\":\"2023-09-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/88/09/KONI_12_2259212.PMC10515676.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Oncoimmunology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/2162402X.2023.2259212\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oncoimmunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/2162402X.2023.2259212","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

抗血管生成疗法是对抗免疫抑制肿瘤微环境(TME)和提高抗肿瘤免疫力的公认方法。PB101是一种基于VEGFR1骨架的糖基化诱饵受体,以高亲和力结合VEGF-a和PlGF。在这里,我们阐明了PB101诱导的肿瘤血管生成和免疫的重塑,它增强了抗PD-L1免疫检查点阻断。PB101通过抑制血管生成和增强CD8+T细胞向肿瘤的浸润来抑制肿瘤生长。PB101诱导抗肿瘤免疫的强大重编程,并激活肿瘤内CD8+T细胞。PB101的抗肿瘤作用主要依赖于CD8+T细胞和IFN-γ。PB101以不同于常规VEGF诱饵受体VEGF陷阱的方式重新编程肿瘤免疫。PB101具有强大的免疫调节能力,与抗PD-L1协同作用,引发增强的抗肿瘤免疫。结合PB101和抗PD-L1可以建立持久的抗肿瘤复发和转移的保护性免疫。这项研究的发现为PB101的进一步临床开发提供了科学依据,特别是当与免疫检查点抑制剂联合使用时,作为晚期癌症的潜在治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

PB101, a VEGF- and PlGF-targeting decoy protein, enhances antitumor immunity and suppresses tumor progression and metastasis.

PB101, a VEGF- and PlGF-targeting decoy protein, enhances antitumor immunity and suppresses tumor progression and metastasis.

PB101, a VEGF- and PlGF-targeting decoy protein, enhances antitumor immunity and suppresses tumor progression and metastasis.

PB101, a VEGF- and PlGF-targeting decoy protein, enhances antitumor immunity and suppresses tumor progression and metastasis.

Antiangiogenic therapy is a recognized method for countering the immunosuppressive tumor microenvironment (TME) and improving anti-tumor immunity. PB101 is a glycosylated decoy receptor that binds to VEGF-A and PlGF with high affinity, based on the VEGFR1 backbone. Here, we elucidated PB101-induced remodeling of tumor angiogenesis and immunity, which enhances anti-PD-L1 immune checkpoint blockade. PB101 inhibited tumor growth by suppressing angiogenesis and enhancing CD8+ T cell infiltration into the tumors. PB101 induced robust reprogramming of antitumor immunity and activates intratumoral CD8+ T cells. Anti-tumor efficacy of PB101 is mostly dependent on CD8+ T cells and IFN-γ. PB101 reprograms tumor immunity in a manner distinct from that of the conventional VEGF decoy receptor, VEGF-trap. With its potent immune-modulating capability, PB101 synergizes with an anti-PD-L1, triggering strengthened antitumor immunity. Combining PB101 and anti-PD-L1 could establish durable protective immunity against tumor recurrence and metastasis. The findings of this study offer scientific rationales for further clinical development of PB101, particularly when used in combination with immune checkpoint inhibitors, as a potential treatment for advanced cancers.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Oncoimmunology
Oncoimmunology ONCOLOGY-IMMUNOLOGY
CiteScore
12.80
自引率
2.80%
发文量
276
期刊介绍: Tumor immunology explores the natural and therapy-induced recognition of cancers, along with the complex interplay between oncogenesis, inflammation, and immunosurveillance. In response to recent advancements, a new journal, OncoImmunology, is being launched to specifically address tumor immunology. The field has seen significant progress with the clinical demonstration and FDA approval of anticancer immunotherapies. There's also growing evidence suggesting that many current chemotherapeutic agents rely on immune effectors for their efficacy. While oncologists have historically utilized chemotherapeutic and radiotherapeutic regimens successfully, they may have unwittingly leveraged the immune system's ability to recognize tumor-specific antigens and control cancer growth. Consequently, immunological biomarkers are increasingly crucial for cancer prognosis and predicting chemotherapy efficacy. There's strong support for combining conventional anticancer therapies with immunotherapies. OncoImmunology will welcome high-profile submissions spanning fundamental, translational, and clinical aspects of tumor immunology, including solid and hematological cancers, inflammation, and both innate and acquired immune responses.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信