ReviewVirulence
Antagonistic crosstalk between type I and II interferons and increased host susceptibility to bacterial infections.
Review in Virulence. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 62 citations in OpenAlex.
- Safety and Immunogenicity of the Recombinant BCG Vaccine AERAS-422 in Healthy BCG-naïve Adults: A Randomized, Active-controlled, First-in-human Phase 1 Trial.EBioMedicine · 2016Trial
- Progress in brucellosis immune regulation inflammatory mechanisms and diagnostic advances.European journal of medical research · 2025Review
- The Role of Type I Interferons in Tuberculosis and in Tuberculosis-Risk-Associated Comorbidities.Infectious disease reports · 2025Review
- Innate immunity in rickettsial infections.Frontiers in cellular and infection microbiology · 2023Review
- Malaria abrogates O'nyong-nyong virus pathologies by restricting virus infection in nonimmune cells.Life science alliance · 2022Article
- Inhibition of macrophage histone demethylase JMJD3 protects against abdominal aortic aneurysms.The Journal of experimental medicine · 2021Article
- Encephalitozoon cuniculi takes advantage of efferocytosis to evade the immune response.PloS one · 2021Article
- Pathogenic Biohacking: Induction, Modulation and Subversion of Host Transcriptional Responses byToxins · 2020Review
- Myeloid Cell CK2 Regulates Inflammation and Resistance to Bacterial Infection.Frontiers in immunology · 2020Article
- The Histone Methyltransferase Setdb2 Modulates Macrophage Phenotype and Uric Acid Production in Diabetic Wound Repair.Immunity · 2019Article
- Effects of type I interferons in malaria.Immunology · 2018Review
- Down regulation of macrophage IFNGR1 exacerbates systemic L. monocytogenes infection.PLoS pathogens · 2017Article
- Transcriptional Profiling in Experimental Visceral Leishmaniasis Reveals a Broad Splenic Inflammatory Environment that Conditions Macrophages toward a Disease-Promoting Phenotype.PLoS pathogens · 2017Article
- Bacterial RNA as a signal to eukaryotic cells as part of the infection process.Discoveries (Craiova, Romania) · 2016Review
- Giving CD4+ T cells the slip: viral interference with MHC class II-restricted antigen processing and presentation.Current opinion in immunology · 2016Review
- Article
- The Dialogue of the Host-Parasite Relationship: Leishmania spp. and Trypanosoma cruzi Infection.BioMed research international · 2015Review
- Article
- Crosstalk between Mycobacterium tuberculosis and the host cell.Seminars in immunology · 2014Review
- Stat1 negatively regulates immune-mediated injury with Anaplasma phagocytophilum infection.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Type I and II interferons (IFNs αβ and γ) have opposing effects on immune resistance to certain pathogenic bacteria. While IFNγ generally plays a protective role, IFNαβ exacerbates Listeria monocytogenes and Mycobacterium tuberculosis infections. Our findings provided evidence that this increased susceptibility reflects a novel antagonistic cross talk between IFNαβ and IFNγ. Macrophages infected with L. monocytogenes strains that induce IFNαβ production responded poorly to IFNγ, as measured by reduced phosphorylation of STAT1 and reduced IFNγ-dependent gene expression. The impaired responsiveness to IFNγ correlated with reduced expression of its receptor, IFNGR, by both infected and bystander macrophages. Down regulation of IFNGR was dependent on responsiveness to IFNγ and mimicked by recombinant IFNβ. Mice lacking responsiveness to IFNαβ (IFNAR1 (-/-)) retained high IFNGR expression, developed higher expression of MHC-II on macrophages and DCs, and were more resistant to systemic L. monocytogenes infection--but only in the presence of IFNγ. Thus, the ability of IFNαβ to down regulate IFNGR provides an explanation for its ability to reduce responsiveness to IFNγ and to increase host susceptibility to bacterial infection. It remains to be determined whether and how such antagonistic interferon crosstalk benefits the host.
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.