ArticleProceedings of the National Academy of Sciences of the United States of America2012
CD14 cooperates with complement receptor 3 to mediate MyD88-independent phagocytosis of Borrelia burgdorferi.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 75 citations in OpenAlex.
- Human TLR8 is activated upon recognition of Borrelia burgdorferi RNA in the phagosome of human monocytes.Journal of leukocyte biology · 2013Trial
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- Royal jelly fermented by honeybee queen (Apis mellifera)-derived Lactobacillus panisapium M1 enhances macrophage phagocytosis through the TLR2/MAPK/SR signaling pathway.BMC complementary medicine and therapies · 2025Article
- Gingipains protect Porphyromonas gingivalis from macrophage-mediated phagocytic clearance.PLoS pathogens · 2025Article
- Phagocytosis via complement receptor 3 enables microbes to evade killing by neutrophils.Journal of leukocyte biology · 2023Article
- Immunization against Zika by entrapping live virus in a subcutaneous self-adjuvanting hydrogel.Nature biomedical engineering · 2023Article
- TREM2 Regulates the Removal of Apoptotic Cells and Inflammatory Processes during the Progression of NAFLD.Cells · 2023Article
- The type of anticoagulant used for plasma collection affects in vitro Rhodococcus equi assays.BMC research notes · 2022Article
- Molecular Mechanisms ofBiology · 2021Review
- Macrophage mediated recognition and clearance of Borrelia burgdorferi elicits MyD88-dependent and -independent phagosomal signals that contribute to phagocytosis and inflammation.BMC immunology · 2021Article
- Constitutive immune mechanisms: mediators of host defence and immune regulation.Nature reviews. Immunology · 2021Review
- Recent Progress in Lyme Disease and Remaining Challenges.Frontiers in medicine · 2021Review
- Borrelia burgdorferi infection induces long-term memory-like responses in macrophages with tissue-wide consequences in the heart.PLoS biology · 2021Article
- Immune Response toCurrent issues in molecular biology · 2021Article
- A combined transcriptomic approach to identify candidates for an anti-tick vaccine blocking B. afzelii transmission.Scientific reports · 2020Article
- Distinct Contributions of CD18 Integrins for Binding and Phagocytic Internalization of Pseudomonas aeruginosa.Infection and immunity · 2020Article
- TLR Agonists as Mediators of Trained Immunity: Mechanistic Insight and Immunotherapeutic Potential to Combat Infection.Frontiers in immunology · 2020Review
- Regulation of macrophage activity by surface receptors contained within Borrelia burgdorferi-enriched phagosomal fractions.PLoS pathogens · 2019Article
- SNX3 drives maturation ofThe Journal of cell biology · 2019Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Phagocytosis of Borrelia burgdorferi, the causative agent of Lyme disease, is a poorly understood process, despite its importance during the host immune response to infection. B. burgdorferi has been shown to bind to different receptors on the surface of phagocytic cells, including the β(2) integrin, complement receptor 3 (CR3). However, whether these receptors mediate the phagocytosis of the spirochete remains unknown. We now demonstrate that CR3 mediates the phagocytosis of the spirochete by murine macrophages and human monocytes. Interaction of B. burgdorferi with the integrin is not sufficient, however, to internalize the spirochete; phagocytosis requires the interaction of CR3 with the GPI-anchored protein, CD14, independently of TLR/MyD88-induced or inside-out signals. Interestingly, the absence of CR3 leads to marked increases in the production of TNF in vitro and in vivo, despite reduced spirochetal uptake. Furthermore, the absence of CR3 during infection with B. burgdorferi results in the inefficient control of bacterial burdens in the heart and increased Lyme carditis. Overall, our data identify CR3 as a MyD88-independent phagocytic receptor for B. burgdorferi that also participates in the modulation of the proinflammatory output of macrophages. These data also establish a unique mechanism of CR3-mediated phagocytosis that requires the direct cooperation of GPI-anchored proteins.
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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.