ArticleJournal of immunology (Baltimore, Md. : 1950)2013
MyD88 signaling in CD4 T cells promotes IFN-γ production and hematopoietic progenitor cell expansion in response to intracellular bacterial infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 43 citations in OpenAlex.
- Impact ofFrontiers in immunology · 2024Article
- The role of inflammation in hematopoiesis and bone marrow failure: What can we learn from mouse models?Frontiers in immunology · 2022Review
- Toll-Like Receptor Signaling and Its Role in Cell-Mediated Immunity.Frontiers in immunology · 2022Review
- Mercury Chloride Impacts on the Development of Erythrocytes and Megakaryocytes in Mice.Toxics · 2021Article
- Episodic Aspiration with Oral Commensals Induces a MyD88-dependent, Pulmonary T-Helper Cell Type 17 Response that Mitigates Susceptibility toAmerican journal of respiratory and critical care medicine · 2021Article
- Macrophages Orchestrate Hematopoietic Programs and Regulate HSC Function During Inflammatory Stress.Frontiers in immunology · 2020Review
- Myeloid differentiation factor 88 signaling in donor T cells accelerates graft-Haematologica · 2020Article
- A Diagnostic Tool for Identification of Etiologies of Fever of Unknown Origin in Adult Patients.Current medical science · 2019Article
- Hematopoietic stem cell loss and hematopoietic failure in severe aplastic anemia is driven by macrophages and aberrant podoplanin expression.Haematologica · 2018Article
- Type I IFNs drive hematopoietic stem and progenitor cell collapse via impaired proliferation and increased RIPK1-dependent cell death during shock-like ehrlichial infection.PLoS pathogens · 2018Article
- VIPER regulates naive T cell activation and effector responses: Implication in TLR4 associated acute stage T cell responses.Scientific reports · 2018Article
- Endogenous Stem Cells in Homeostasis and Aging.Tissue engineering and regenerative medicine · 2017Article
- TNF signalling drives expansion of bone marrow CD4+ T cells responsible for HSC exhaustion in experimental visceral leishmaniasis.PLoS pathogens · 2017Article
- Major Histocompatibility Complex Class II HLA-DRα Is Downregulated by Kaposi's Sarcoma-Associated Herpesvirus-Encoded Lytic Transactivator RTA and MARCH8.Journal of virology · 2016Article
- Ehrlichioses: An Important One Health Opportunity.Veterinary sciences · 2016Review
- Hypercholesterolemia Tunes Hematopoietic Stem/Progenitor Cells for Inflammation and Atherosclerosis.International journal of molecular sciences · 2016Review
- MyD88 Mediates Instructive Signaling in Dendritic Cells and Protective Inflammatory Response during Rickettsial Infection.Infection and immunity · 2016Article
- Macrophages: Key regulators of steady-state and demand-adapted hematopoiesis.Experimental hematology · 2016Review
- FcγRIIIa-Syk Co-signal Modulates CD4+ T-cell Response and Up-regulates Toll-like Receptor (TLR) Expression.The Journal of biological chemistry · 2016Article
- Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia.Frontiers in immunology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Hematopoietic stem and progenitor cell (HSPC) phenotype and function can change in response to infectious challenge. These changes can be mediated by cytokines, IFNs, and pathogen-associated molecules, via TLR, and are thought to promote tailored immune responses for particular pathogens. In this study, we investigated the signals that activate HSPCs during ehrlichiosis, a disease characterized by profound hematopoietic dysfunction in both humans and mice. In a mouse model of ehrlichiosis, we observed that infection-induced proliferation of bone marrow HSPCs was dependent on IFN-γ signaling and was partially dependent on MyD88. However, MyD88 was not required in HSPCs for their expansion during infection, because similar frequencies of MyD88-deficient and wild-type HSPCs proliferated in mixed bone marrow chimeric mice. MyD88-deficient mice exhibited low serum and bone marrow concentration of IFN-γ compared with wild-type mice. We next identified CD4 T cells as the primary cells producing IFN-γ in the bone marrow and demonstrated a nonredundant role for CD4-derived IFN-γ in increased HSPCs. Using mixed bone marrow chimeric mice, we identified a requirement for MyD88 in CD4 T cells for increased T-bet expression, optimal IFN-γ production, and CD4 T cell proliferation. Our data demonstrate an essential role for CD4 T cells in mediating HSPC activation in response to bacterial infection and illustrate a novel role for MyD88 signaling in CD4 T cells in this process. These findings further support the idea that IFN-γ production is essential for HSPC activation and hematopoietic responses to infection.
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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.