دورية أكاديمية
Formyl peptide enhances cancer immunotherapy by activating antitumoral neutrophils, and T cells.
| العنوان: | Formyl peptide enhances cancer immunotherapy by activating antitumoral neutrophils, and T cells. |
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| المؤلفون: | Sun H; State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou,Guangdong 510060, China; Department of Pharmacy, Shenzhen Third People's Hospital, Shenzhen, Guangdong Province 518112, China., Li S; State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou,Guangdong 510060, China., Wang Q; State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou,Guangdong 510060, China., Luo C; Guangxi Hospital Division of The First Affiliated Hospital, Sun Yat-Sen University, Nanning 530022, China., Zhong L; State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou,Guangdong 510060, China., Wan G; School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, China., Li Z; State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou,Guangdong 510060, China., Zhao G; State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou,Guangdong 510060, China., Bu X; School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, China., Zeng M; State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou,Guangdong 510060, China., Feng G; State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Department of Experimental Research, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Sun Yat-sen University, Guangzhou,Guangdong 510060, China. Electronic address: fengguok@sysucc.org.cn. |
| المصدر: | Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [Biomed Pharmacother] 2024 Jun; Vol. 175, pp. 116670. Date of Electronic Publication: 2024 Apr 30. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Editions Scientifiques Elsevier Country of Publication: France NLM ID: 8213295 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1950-6007 (Electronic) Linking ISSN: 07533322 NLM ISO Abbreviation: Biomed Pharmacother Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Paris : Editions Scientifiques Elsevier Original Publication: New York, N.Y. : Masson Pub. USA, Inc., c1982- |
| مواضيع طبية MeSH: | Neutrophils*/drug effects , Neutrophils*/immunology , Neutrophils*/metabolism , Tumor Microenvironment*/drug effects , Tumor Microenvironment*/immunology , Immunotherapy*/methods , Receptors, Formyl Peptide*/metabolism , T-Lymphocytes*/immunology , T-Lymphocytes*/drug effects , Mice, Inbred C57BL*, Animals ; Mice ; Cell Line, Tumor ; Reactive Oxygen Species/metabolism ; Humans ; Female ; Neutrophil Activation/drug effects ; Neoplasms/immunology ; Neoplasms/drug therapy ; Neoplasms/pathology ; Lymphocyte Activation/drug effects ; Programmed Cell Death 1 Receptor/metabolism ; Programmed Cell Death 1 Receptor/immunology |
| مستخلص: | Neutrophils are heterogeneous and plastic, with the ability to polarize from antitumour to protumour phenotype and modulate tumour microenvironment components. While some advances have been made, the neutrophil-targeting therapy remains underexplored. Activation of formyl peptide receptors (FPRs) by formylated peptides is needed for local control of infection through the recruitment of activated neutrophils while the potential contribution of antitumour activity remains underexplored. Here, we demonstrate that neutrophils can be harnessed to suppress tumour growth through the action of the formyl peptide (FP) on the formyl peptide receptor (FPR). Mechanistically, FP efficiently recruits neutrophils to produce reactive oxygen species production (ROS), resulting in the direct killing of tumours. Antitumour functions disappeared when neutrophils were depleted by anti-Ly6G antibodies. Interestingly, extensive T-cell activation was observed in mouse tumours treated with FP, showing the potential to alter the immune suppressed tumour microenvironment (TME) and further sensitize mice to anti-PD1 therapy. Transcriptomic and flow cytometry analyses revealed the mechanisms of FP-sensitized anti-PD1 therapy, mainly including stimulated neutrophils and an altered immune-suppressed tumour microenvironment. Collectively, these data establish FP as an effective combination partner for sensitizing anti-PD1 therapy by stimulating tumour-infiltrated neutrophils. Competing Interests: Declaration of Competing Interest The authors declare no potential conflicts of interest. (Copyright © 2024. Published by Elsevier Masson SAS.) |
| فهرسة مساهمة: | Keywords: Formyl peptide; Immunotherapy; Neutrophils; T-cell; Tumour microenvironment |
| المشرفين على المادة: | 0 (Receptors, Formyl Peptide) 0 (Reactive Oxygen Species) 0 (Programmed Cell Death 1 Receptor) |
| تواريخ الأحداث: | Date Created: 20240501 Date Completed: 20240602 Latest Revision: 20240602 |
| رمز التحديث: | 20240602 |
| DOI: | 10.1016/j.biopha.2024.116670 |
| PMID: | 38692065 |
| قاعدة البيانات: | MEDLINE |
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Full Text Finder | تدمد: | 1950-6007 |
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| DOI: | 10.1016/j.biopha.2024.116670 |