ArticlePloS one2010
MyD88-dependent signaling contributes to host defense against ehrlichial infection.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 40 citations in OpenAlex.
- Know Your ABCs: Discovery, Differentiation, and Targeting of T-Bet+ B Cells.Immunological reviews · 2025Review
- T-betJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Sterile alpha and TIR motif-containing protein 1 is a negative regulator in the anti-bacterial immune responses in nile tilapia (Frontiers in immunology · 2022Article
- Comparative Analysis of Genome of Ehrlichia sp. HF, a Model Bacterium to Study Fatal Human Ehrlichiosis.BMC genomics · 2021Article
- Pattern Recognition Receptors in Innate Immunity to Obligate Intracellular Bacteria.Zoonoses (Shannon, Ireland) · 2021Article
- Article
- Discovery ofFrontiers in cellular and infection microbiology · 2020Article
- The Prostaglandin E2-EP3 Receptor Axis Regulates Anaplasma phagocytophilum-Mediated NLRC4 Inflammasome Activation.PLoS pathogens · 2016Article
- MyD88 Mediates Instructive Signaling in Dendritic Cells and Protective Inflammatory Response during Rickettsial Infection.Infection and immunity · 2016Article
- MyD88 signaling in CD4 T cells promotes IFN-γ production and hematopoietic progenitor cell expansion in response to intracellular bacterial infection.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humans.European journal of immunology · 2012Review
- Cutting edge: impaired MHC class I expression in mice deficient for Nlrc5/class I transactivator.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Penicillin-binding protein of Ehrlichia chaffeensis: cytokine induction through MyD88-dependent pathway.The Journal of infectious diseases · 2012Article
- Intracellular invasion of Orientia tsutsugamushi activates inflammasome in asc-dependent manner.PloS one · 2012Article
- Hair-Loss Preventing Effect of Grateloupia elliptica.Biomolecules & therapeutics · 2012Article
- Ehrlichia chaffeensis induces monocyte inflammatory responses through MyD88, ERK, and NF-κB but not through TRIF, interleukin-1 receptor 1 (IL-1R1)/IL-18R1, or toll-like receptors.Infection and immunity · 2011Article
- Mechanisms of obligatory intracellular infection with Anaplasma phagocytophilum.Clinical microbiology reviews · 2011Review
- Molecular and cellular pathobiology of Ehrlichia infection: targets for new therapeutics and immunomodulation strategies.Expert reviews in molecular medicine · 2011Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The ehrlichiae are small gram-negative obligate intracellular bacteria in the family Anaplasmataceae. Ehrlichial infection in an accidental host may result in fatal diseases such as human monocytotropic ehrlichiosis, an emerging, tick-borne disease. Although the role of adaptive immune responses in the protection against ehrlichiosis has been well studied, the mechanism by which the innate immune system is activated is not fully understood. Using Ehrlichia muris as a model organism, we show here that MyD88-dependent signaling pathways play a pivotal role in the host defense against ehrlichial infection. Upon E. muris infection, MyD88-deficient mice had significantly impaired clearance of E. muris, as well as decreased inflammation, characterized by reduced splenomegaly and recruitment of macrophages and neutrophils. Furthermore, MyD88-deficient mice produced markedly lower levels of IL-12, which correlated well with an impaired Th1 immune response. In vitro, dendritic cells, but not macrophages, efficiently produced IL-12 upon E. muris infection through a MyD88-dependent mechanism. Therefore, MyD88-dependent signaling is required for controlling ehrlichial infection by playing an essential role in the immediate activation of the innate immune system and inflammatory cytokine production, as well as in the activation of the adaptive immune system at a later stage by providing for optimal Th1 immune responses.
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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.