ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Downstream signals for MyD88-mediated phagocytosis of Borrelia burgdorferi can be initiated by TRIF and are dependent on PI3K.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Endosome restricted human TLR1 polymorphism highlights a role for MyD88 in Pam3CSK4 detection.PloS one · 2026Article
- Primordial germ cell-derived macrophages as a platform to study host-pathogen interactions.Frontiers in cell and developmental biology · 2026Article
- Azithromycin Augments Bacterial Uptake and Anti-Inflammatory Macrophage Polarization in Cystic Fibrosis.Cells · 2024Article
- A genome-wide screen in macrophages identifies PTEN as required for myeloid restriction of Listeria monocytogenes infection.PLoS pathogens · 2023Article
- Molecular characterization and functional analysis of DIGIRR from golden pompano (Frontiers in immunology · 2022Article
- Molecular Mechanisms ofBiology · 2021Review
- Polymicrobial communities in periodontal disease: Their quasi-organismal nature and dialogue with the host.Periodontology 2000 · 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
- SNX3 drives maturation ofThe Journal of cell biology · 2019Article
- Phagocytic Receptors Activate Syk and Src Signaling during Borrelia burgdorferi Phagocytosis.Infection and immunity · 2017Article
- MyD88 in Mycobacterium tuberculosis infection.Medical microbiology and immunology · 2017Review
- Infection with the Lyme disease pathogen suppresses innate immunity in mice with diet-induced obesity.Cellular microbiology · 2017Article
- Article
- Tick sialostatins L and L2 differentially influence dendritic cell responses to Borrelia spirochetes.Parasites & vectors · 2015Article
- Mechanisms of Borrelia burgdorferi internalization and intracellular innate immune signaling.Frontiers in cellular and infection microbiology · 2014Review
- Phagosomal TLR signaling upon Borrelia burgdorferi infection.Frontiers in cellular and infection microbiology · 2014Review
- The formins FMNL1 and mDia1 regulate coiling phagocytosis of Borrelia burgdorferi by primary human macrophages.Infection and immunity · 2013Article
- TRIF mediates Toll-like receptor 2-dependent inflammatory responses to Borrelia burgdorferi.Infection and immunity · 2013Article
- CD14 targets complement receptor 3 to lipid rafts during phagocytosis of Borrelia burgdorferi.International journal of biological sciences · 2013Article
- CD14 cooperates with complement receptor 3 to mediate MyD88-independent phagocytosis of Borrelia burgdorferi.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
We previously have shown that MyD88 is important for uptake of Borrelia burgdorferi by bone marrow derived macrophages (BMDMs). The mechanism by which MyD88 is involved in uptake of B. burgdorferi is currently is not well characterized. Here, we report that MyD88-mediated defect in the phagocytosis of B. burgdorferi can be complemented by TLR3/Toll/IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) activation in BMDMs from MyD88(-/-) mice. This effect of TLR3/TRIF activation was not due to its induction of type I IFNs, suggesting instead a convergence of signaling pathways downstream of MyD88 and TRIF. To characterize signaling pathways involved in MyD88-mediated phagocytosis of B. burgdorferi, BMDMs were treated with specific inhibitors of MAPK, protein kinase C, JAK/STAT, or PI3K. Only inhibition of PI3K resulted in a significant decrease of B. burgdorferi uptake. Consistent with this, B. burgdorferi activation of MyD88 or TLR3/TRIF signaling resulted in increased activity of PI3K. Additionally, association of B. burgdorferi with actin-related protein (Arp2/3) complexes, which facilitate actin rearrangements during phagocytosis, was similarly reduced in MyD88(-/-) BMDMs and in BMDMs treated with a PI3K inhibitor. Taken together, these findings define an essential pathway whereby downstream signals from MyD88 or TRIF converge on PI3K, which triggers actin polymerization to initiate the phagocytosis of B. burgdorferi.
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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.