ArticleJournal of immunology (Baltimore, Md. : 1950)2017
Inactivation of Rab11a GTPase in Macrophages Facilitates Phagocytosis of Apoptotic Neutrophils.
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Antibody-lectin chimeras for glyco-immune checkpoint blockade.Nature biotechnology · 2026Article
- Skin-mimetic bilayer hydrogel normalizes diabetic wound healing by orchestrating inflammatory cell dynamics: An early intervention strategy.Bioactive materials · 2026Article
- Indole-acetaldehyde from Rothia mucilaginosa activates the PXR/NRF2 axis to enhance alveolar macrophage phagocytosis and protect against ARDS.Respiratory research · 2026Article
- Macrophage efferocytosis mediated by the TP63-RAC2 pathway promotes immunosuppressive remodeling in esophageal cancer.Cell reports. Medicine · 2026Article
- Rab43 mitigates the inflammatory response in acute lung injury via MyD88 ubiquitination.Scientific reports · 2026Article
- Rab11b is necessary for mitochondrial integrity and function in gut epithelial cells.Frontiers in cell and developmental biology · 2025Article
- Extracellular histones promote TWIK2-dependent potassium efflux and associated NLRP3 activation in alveolar macrophages during sepsis-induced lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Enhanced T-cell activation and chemokine-associated function in CD14-positive cells from venous sinus blood in sub-acute cerebral venous sinus thrombosis.Frontiers in cell and developmental biology · 2024Article
- Lidocaine pretreatment attenuates inflammatory response and protects against sepsis-induced acute lung injury via inhibiting potassium efflux-dependent NLRP3 activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Endosomal trafficking of two-pore KeLife · 2023Article
- BIGKnock: fine-mapping gene-based associations via knockoff analysis of biobank-scale data.Genome biology · 2023Article
- Cellular mechanisms underlying the impairment of macrophage efferocytosis.Immunology letters · 2023Review
- Wun2-mediated integrin recycling promotes apoptotic cell clearance in Drosophila melanogaster.Cell death and differentiation · 2022Article
- Pleiotropic Roles of Scavenger Receptors in Circadian Retinal Phagocytosis: A New Function for Lysosomal SR-B2/LIMP-2 at the RPE Cell Surface.International journal of molecular sciences · 2022Article
- Extracellular HMGB1 Impairs Macrophage-Mediated Efferocytosis by Suppressing the Rab43-Controlled Cell Surface Transport of CD91.Frontiers in immunology · 2022Article
- SIRT2-PFKP interaction dysregulates phagocytosis in macrophages with acute ethanol-exposure.Frontiers in immunology · 2022Article
- TLR4 is required for macrophage efferocytosis during resolution of ventilator-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Rab GTPases in the differential processing of phagocytosed pathogens versus efferocytosed apoptotic cells.Histology and histopathology · 2021Review
- Review
- Introduction to the Community of Extracellular Vesicles.Sub-cellular biochemistry · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The timely and efficient clearance of apoptotic neutrophils by macrophages (efferocytosis) is required for the resolution of inflammation and tissue repair, but the regulatory mechanisms remain unclear. In this study, we investigated the role of the small GTPase Ras-related protein in brain (Rab)11a in regulating efferocytosis, and on this basis the resolution of inflammatory lung injury. We observed that apoptotic neutrophil feeding induced a rapid loss of Rab11a activity in bone marrow-derived macrophages and found that depletion of Rab11a in macrophages by small interfering RNA dramatically increased the phagocytosis of apoptotic neutrophils compared with control cells. Additionally, overexpression of wild-type Rab11a inhibited macrophage efferocytosis, whereas overexpression of dominant-negative Rab11a (Rab11a S25N) increased the clearance of apoptotic neutrophils. Rab11a knockdown also increased the surface level of CD36 in macrophages, but it reduced cell surface expression of a disintegrin and metalloproteinase (ADAM) 17. Depletion of ADAM17 rescued the decreased surface CD36 expression found in macrophages overexpressing wild-type Rab11a. Also, blockade of CD36 abolished the augmented efferocytosis seen in Rab11a-depleted macrophages. In mice challenged with endotoxin, intratracheal instillation of Rab11a-depleted macrophages reduced neutrophil count in bronchoalveolar lavage fluid, increased the number of macrophages containing apoptotic neutrophils, and prevented inflammatory lung injury. Thus, Rab11a inactivation in macrophages as a result of apoptotic cell binding initiates phagocytosis of apoptotic neutrophils via the modulation of ADAM17-mediated CD36 cell surface expression. Our results raise the possibility that inhibition of Rab11a activity in macrophages is a promising strategy for activating the resolution of inflammatory lung injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.