ArticleThe American journal of pathology2012
Contribution of NK cells to the innate phase of host protection against an intracellular bacterium targeting systemic endothelium.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- A humanized IFN-γ mouse model reveals skin eschar formation, enhanced susceptibility and scrub typhus pathogenesis.PLoS pathogens · 2026Article
- Development of a rapid antigen-based lateral flow assay for tick-borne spotted fever rickettsioses.PloS one · 2025Article
- Lack of the IFN-γ signal leads to lethal Orientia tsutsugamushi infection in mice with skin eschar lesions.PLoS pathogens · 2024Article
- Innate immunity in rickettsial infections.Frontiers in cellular and infection microbiology · 2023Review
- Review
- Review
- Contribution of classical complement activation and IgM to the control of Rickettsia infection.Molecular microbiology · 2021Article
- MicroRNA-424 regulates the expression of CX3CL1 (fractalkine) in human microvascular endothelial cells duringBiochemistry and biophysics reports · 2021Article
- Subversion of Host Innate Immunity byFrontiers in immunology · 2021Article
- Review
- Neuroinflammation associated with scrub typhus and spotted fever group rickettsioses.PLoS neglected tropical diseases · 2020Review
- Innate Immune Response to Tick-Borne Pathogens: Cellular and Molecular Mechanisms Induced in the Hosts.International journal of molecular sciences · 2020Review
- Activation of ASC Inflammasome Driven by Toll-Like Receptor 4 Contributes to Host Immunity against Rickettsial Infection.Infection and immunity · 2020Article
- Global Transcriptomic Profiling of Pulmonary Gene Expression in an Experimental Murine Model ofGenes · 2019Article
- Pathogenesis of Rickettsial Diseases: Pathogenic and Immune Mechanisms of an Endotheliotropic Infection.Annual review of pathology · 2019Review
- Vector Tick Transmission Model of Spotted Fever Rickettsiosis.The American journal of pathology · 2019Article
- Article
- Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies.Journal of immunology research · 2019Review
- Immune response against rickettsiae: lessons from murine infection models.Medical microbiology and immunology · 2017Review
- Increased level and interferon-γ production of circulating natural killer cells in patients with scrub typhus.PLoS neglected tropical diseases · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We investigated the mechanisms by which natural killer (NK) cells mediate innate host defense against infection with an endothelium-targeting intracellular bacterium, Rickettsia. We found that a robust Rickettsia-induced innate response in resistant mice cleared the bacteria early in the infection and was associated with significantly higher frequencies of splenic interferon (IFN)-γ (+) CD8(+) T cells and cytotoxic NK cells compared with susceptible mice. More importantly, NK cell-deficient Rag(-/-)γc(-/-) animals displayed significantly increased susceptibility to Rickettsia infection compared with NK cell-sufficient Rag(-/-) mice, as evidenced by impaired bacterial clearance, early development of severe thrombosis in the liver, and a decreased serum level of IFN-γ. Furthermore, the lack of NK cells also impaired host resistance of CB-17 scid mice to Rickettsia, similar to what was observed in Rag(-/-)γc(-/-) mice. Interestingly, perforin deficiency in Rag(-/-)Prf1(-/-) mice resulted in greater thrombosis and insignificantly different systemic levels of IFN-γ compared with Rag(-/-) mice, suggesting that perforin, which is mainly produced by NK cells, is involved in the prevention of vascular damage. Together, these findings reveal that NK cells mediate the innate phase of host protection against infection with rickettsiae, most likely via IFN-γ production. Furthermore, NK cells are involved in preventing rickettsial infection-induced endothelial cell damage, possibly via perforin production.
Indexed as
Identifiers
What OpenQuestion holds
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.