ArticleInfection and immunity1992
Poly(I.C)-induced interferons enhance susceptibility of SCID mice to systemic candidiasis.
Article in Infection and immunity, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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
13 citing papers in PubMed, 38 citations in OpenAlex.
- Myeloid Cell Diversity and Impact of Metabolic Cues during Atherosclerosis.Immunometabolism · 2020Article
- Type I Interferons Ameliorate Zinc Intoxication of Candida glabrata by Macrophages and Promote Fungal Immune Evasion.iScience · 2020Article
- Role of type I interferons in inflammasome activation, cell death, and disease during microbial infection.Frontiers in cellular and infection microbiology · 2013Review
- Type I IFN-mediated regulation of IL-1 production in inflammatory disorders.Cellular and molecular life sciences : CMLS · 2012Review
- T cells augment monocyte and neutrophil function in host resistance against oropharyngeal candidiasis.Infection and immunity · 2001Article
- Intestinal lesions associated with disseminated candidiasis in an experimental animal model.Journal of clinical microbiology · 2000Article
- Macrophages in resistance to candidiasis.Microbiology and molecular biology reviews : MMBR · 1997Review
- Production and function of cytokines in natural and acquired immunity to Candida albicans infection.Microbiological reviews · 1995Review
- Gamma delta T cell-induced nitric oxide production enhances resistance to mucosal candidiasis.Nature medicine · 1995Article
- A T cell-independent protective host response against Cryptococcus neoformans expressed at the primary site of infection in the lung.Infection and immunity · 1993Article
- Natural killer cells do not play a dominant role in CD4+ subset differentiation in Candida albicans-infected mice.Infection and immunity · 1993Article
- Enhancement of susceptibility of CB-17 mice to systemic candidiasis by poly(I . C)-induced interferon.Infection and immunity · 1993Article
- Effect of abrogation of natural killer cell activity on the course of candidiasis induced by intraperitoneal administration and gastrointestinal candidiasis in mice with severe combined immunodeficiency.Infection and immunity · 1993Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In the absence of any demonstrable T- or B-cell responses, gnotobiotic CB-17 SCID (severe combined immunodeficient) mice not only show innate resistance to acute systemic (intravenous challenge) candidiasis but also manifest innate resistance to systemic candidiasis of endogenous (gastrointestinal tract) origin. Poly(I. C), a potent inducer of interferons (IFNs) in vivo, enhanced the susceptibility of CB-17 SCID mice to acute systemic candidiasis and to systemic candidiasis of endogenous origin, as demonstrated by increased numbers of viable Candida albicans in internal organs after poly(I. C) treatment. The poly(I. C)-enhanced susceptibility of mice to candidiasis was abrogated by in vivo treatment with antibodies to IFN-alpha, -beta, and -gamma. In vivo depletion of natural killer cells from SCID mice did not significantly enhance their susceptibility to systemic candidiasis or abrogate poly(I. C)-enhanced susceptibility. In vivo and in vitro, treatment with poly(I. C) impaired the candidacidal and phagocytic activity of thioglycollate-elicited macrophages from SCID mice. Antibody to IFN-alpha/beta or IFN-beta alone interfered with the ability of poly(I. C) to impair the candidacidal activity of macrophages from SCID mice in vitro. These data suggest that poly(I. C)-induced interferons can impair the candidacidal activity of macrophages in SCID mice and decrease their innate resistance to acute systemic candidiasis and to systemic candidiasis of endogenous origin.
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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.