In situ neutrophil efferocytosis shapes T cell immunity to influenza infection

Early recruitment of neutrophils from the blood to sites of tissue infection is a hallmark of innate immune responses. However, little is known about the mechanisms by which apoptotic neutrophils are cleared in infected tissues during resolution and the immunological consequences of in situ efferocytosis. Using intravital multiphoton microscopy, we show previously unrecognized motility patterns of interactions between neutrophils and tissue-resident phagocytes within the influenza-infected mouse airway. Newly infiltrated inflammatory monocytes become a chief pool of phagocytes and play a key role in the clearance of highly motile apoptotic neutrophils during the resolution phase. Apoptotic neutrophils further release epidermal growth factor and promote the differentiation of monocytes into tissue-resident antigen-presenting cells for activation of antiviral T cell effector functions. Collectively, these results suggest that the presence of in situ neutrophil resolution at the infected tissue is critical for optimal CD8+ T cell-mediated immune protection.

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Kihong Lim, Tae-Hyoun Kim, Alissa Trzeciak, Andrea M Amitrano, Emma C Reilly, Hen Prizant, Deborah J Fowell, David J Topham, Minsoo Kim

期刊 Nat Immunol
影响因子 30.5
起止号 2020 Sep;21(9):1046-1057.
种属 Mouse
技术平台抗体芯片
应用领域呼吸系统
研究方向呼吸系统
细胞类型 T细胞,粒细胞
疾病类型流感
检测蛋白 Adiponectin/Acrp30,DPPIV/CD26,IL-27,Amphiregulin,EGF,IL-28,Angiopoietin-1,Endoglin/CD105,IL-33,Angiopoietin-2,Endostatin,LDL R,Angiopoietin-like 3,Fetuin A/AHSG,Leptin,BAFF/BLyS/TNFSF13B,FGF acidic,LIF,C1q R1/CD93,FGF-21,Lipocalin-2/NGAL,CCL2/JE/MCP-1,Flt-3 Ligand,LIX,CCL3/CCL4 MIP-1 alpha/beta,Gas6,M-CSF,CCL5/RANTES,G-CSF,MMP-2,CCL6/C10,GDF-15,MMP-3,CCL11/Eotaxin,GM-CSF,MMP-9,CCL12/MCP-5,HGF,Myeloperoxidase,CCL17/TARC,ICAM-1/CD54,Osteopontin (OPN),CCL19/MIP-3 beta,IFN-gamma,Osteoprotegerin/TNFRSF11B,CCL20/MIP-3 alpha,IGFBP-1,PD-ECGF/Thymidine phosphorylase,CCL21/6Ckine,IGFBP-2,PDGF-BB,CCL22/MDC,IGFBP-3,Pentraxin 2/SAP,CD14,IGFBP-5,Pentraxin 3/ TSG-14,CD40/TNFRSF5,IGFBP-6,Periostin/OSF-2,CD160,IL-1 alpha/IL1F1,Pref-1/DLK-1/FA1,Chemerin,IL-1 beta/IL-1F2,Proliferin,Chitinase 3-like 1,IL-1ra/IL-1F3,Proprotein Convertase 9/PCSK9,Coagulation Factor III/Tissue Factor,IL-2,RAGE,Complement Component C5/C5a,IL-3,RBP4,Complement Factor D,IL-4,Reg3G,C-Reactive Protein/CRP,IL-5,Resistin,CX3CL1/Fractalkine,IL-6,E-Selectin/CD62E,CXCL1/KC,IL-7,P-Selectin/CD62P,CXCL2/MIP-2,IL-10,Serpin E1/PAI-1,CXCL9/MIG,IL-11,Serpin F1/PEDF,CXCL10/IP-10,IL-12p40,Thrombopoietin,CXCL11/I-TAC,IL-13,TIM-1/KIM-1/HAVCR,CXCL13/BLC/BCA-1,IL-15,TNF-alpha,CXCL16,IL-17A,VCAM-1/CD106,Cystatin C,IL-22,VEGF,Dkk-1,IL-23,WISP-1/CCN4

Abstract

Early recruitment of neutrophils from the blood to sites of tissue infection is a hallmark of innate immune responses. However, little is known about the mechanisms by which apoptotic neutrophils are cleared in infected tissues during resolution and the immunological consequences of in situ efferocytosis. Using intravital multiphoton microscopy, we show previously unrecognized motility patterns of interactions between neutrophils and tissue-resident phagocytes within the influenza-infected mouse airway. Newly infiltrated inflammatory monocytes become a chief pool of phagocytes and play a key role in the clearance of highly motile apoptotic neutrophils during the resolution phase. Apoptotic neutrophils further release epidermal growth factor and promote the differentiation of monocytes into tissue-resident antigen-presenting cells for activation of antiviral T cell effector functions. Collectively, these results suggest that the presence of in situ neutrophil resolution at the infected tissue is critical for optimal CD8+ T cell-mediated immune protection.

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Abstract