ArticleThe American journal of pathology2010
Natural killer cells promote tissue injury and systemic inflammatory responses during fatal Ehrlichia-induced toxic shock-like syndrome.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Efficacy and immunological correlates of an mRNA-LNP vaccine for protection against an emerging rickettsial pathogen.Emerging microbes & infections · 2026Article
- Non-Canonical Inflammasome Pathway: The Role of Cell Death and Inflammation in Ehrlichiosis.Cells · 2023Review
- Article
- Review: Protective Immunity and Immunopathology of Ehrlichiosis.Zoonoses (Shannon, Ireland) · 2022Article
- Effect of GP19 Peptide Hyperimmune Antiserum on Activated Macrophage duringAnimals : an open access journal from MDPI · 2021Article
- Comparative Analysis of Genome of Ehrlichia sp. HF, a Model Bacterium to Study Fatal Human Ehrlichiosis.BMC genomics · 2021Article
- Immune Response to Tick-Borne Hemoparasites: Host Adaptive Immune Response Mechanisms as Potential Targets for Therapies and Vaccines.International journal of molecular sciences · 2020Review
- mTORC1-mediated polarization of M1 macrophages and their accumulation in the liver correlate with immunopathology in fatal ehrlichiosis.Scientific reports · 2019Article
- Emerging Roles of Autophagy and Inflammasome in Ehrlichiosis.Frontiers in immunology · 2019Review
- 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
- Natural killer cells as a therapeutic tool for infectious diseases - current status and future perspectives.Oncotarget · 2018Review
- Antigen-Specific CD4Frontiers in immunology · 2018Article
- MyD88-dependent inflammasome activation and autophagy inhibition contributes to Ehrlichia-induced liver injury and toxic shock.PLoS pathogens · 2017Article
- Memory of Natural Killer Cells: A New Chance againstFrontiers in immunology · 2017Review
- NK Cell-Mediated Regulation of Protective Memory Responses against Intracellular Ehrlichial Pathogens.PloS one · 2016Article
- Type I interferon contributes to noncanonical inflammasome activation, mediates immunopathology, and impairs protective immunity during fatal infection with lipopolysaccharide-negative ehrlichiae.The American journal of pathology · 2015Article
- NK and NKT Cell Depletion Alters the Outcome of Experimental Pneumococcal Pneumonia: Relationship with Regulation of Interferon-γ Production.Journal of immunology research · 2015Article
- Bench-to-bedside review: Natural killer cells in sepsis - guilty or not guilty?Critical care (London, England) · 2013Review
- Neutrophils mediate immunopathology and negatively regulate protective immune responses during fatal bacterial infection-induced toxic shock.Infection and immunity · 2013Article
- TLR2 and Nod2 mediate resistance or susceptibility to fatal intracellular Ehrlichia infection in murine models of ehrlichiosis.PloS one · 2013Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Human monocytotropic ehrlichiosis is caused by Ehrlichia chaffeensis, a Gram-negative bacterium lacking lipopolysaccharide. We have shown that fatal murine ehrlichiosis is associated with CD8(+)T cell-mediated tissue damage, tumor necrosis factor-alpha, and interleukin (IL)-10 overproduction, and CD4(+)Th1 hyporesponsiveness. In this study, we examined the relative contributions of natural killer (NK) and NKT cells in Ehrlichia-induced toxic shock. Lethal ehrlichial infection in wild-type mice induced a decline in NKT cell numbers, and late expansion and migration of activated NK cells to the liver, a main infection site that coincided with development of hepatic injury. The spatial and temporal changes in NK and NKT cells in lethally infected mice correlated with higher NK cell cytotoxic activity, higher expression of cytotoxic molecules such as granzyme B, higher production of interferon-gamma and tumor necrosis factor-alpha, increased hepatic infiltration with CD8alphaCD11c(+) dendritic cells and CD8(+)T cells, decreased splenic CD4(+)T cells, increased serum concentrations of IL-12p40, IL-18, RANTES, and monocyte chemotactic protein-1, and elevated production of IL-18 by liver mononuclear cells compared with nonlethally infected mice. Depletion of NK cells prevented development of severe liver injury, decreased serum levels of interferon-gamma, tumor necrosis factor-alpha, and IL-10, and enhanced bacterial elimination. These data indicate that NK cells promote immunopathology and defective anti-ehrlichial immunity, possibly via decreasing the protective immune response mediated by interferon-gamma producing CD4(+)Th1 and NKT cells.
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