ArticleThe American journal of pathology2000
Interferon-gamma and tumor necrosis factor-alpha determine resistance to Paracoccidioides brasiliensis infection in mice.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 180 citations in OpenAlex.
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- MDSCs use a complex molecular network to suppress T-cell immunity in a pulmonary model of fungal infection.Frontiers in cellular and infection microbiology · 2024Article
- Article
- Myeloid-derived suppressor cells are associated with impaired Th1 and Th17 responses and severe pulmonary paracoccidioidomycosis which is reversed by anti-Gr1 therapy.Frontiers in immunology · 2023Article
- Paracoccidioidomycosis: Current Status and Future Trends.Clinical microbiology reviews · 2022Review
- Paracoccidioidomycosis Protective Immunity.Journal of fungi (Basel, Switzerland) · 2021Review
- Identification of Potentially Therapeutic Immunogenic Peptides FromFrontiers in immunology · 2021Article
- β2 Integrin-Mediated Susceptibility toFrontiers in cellular and infection microbiology · 2021Article
- Advances in Fungal Peptide Vaccines.Journal of fungi (Basel, Switzerland) · 2020Review
- Living Within the Macrophage: Dimorphic Fungal Pathogen Intracellular Metabolism.Frontiers in cellular and infection microbiology · 2020Review
- Caspase-11-dependent IL-1α release boosts Th17 immunity against Paracoccidioides brasiliensis.PLoS pathogens · 2019Article
- Impact ofBioMed research international · 2019Article
- Proteomic Analysis ofFrontiers in microbiology · 2019Article
- Intestinal paracoccidioidomycosis resembling Crohn's disease in a teenager: a case report.Journal of medical case reports · 2018Article
- A Dectin-1-Caspase-8 Pathway Licenses Canonical Caspase-1 Inflammasome Activation and Interleukin-1β Release in Response to a Pathogenic Fungus.The Journal of infectious diseases · 2018Article
- Recombinant vaccines of a CD4+ T-cell epitope promote efficient control of Paracoccidioides brasiliensis burden by restraining primary organ infection.PLoS neglected tropical diseases · 2017Article
- Th17-Inducing Cytokines IL-6 and IL-23 Are Crucial for Granuloma Formation during Experimental Paracoccidioidomycosis.Frontiers in immunology · 2017Article
- Severe Paracoccidioidomycosis in a 14-Year-Old Boy.Mycopathologia · 2016Article
- Tolerogenic Plasmacytoid Dendritic Cells Control Paracoccidioides brasiliensis Infection by Inducting Regulatory T Cells in an IDO-Dependent Manner.PLoS pathogens · 2016Article
- Activation strategies for invariant natural killer T cells.Immunogenetics · 2016Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the role of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in the resistance to Paracoccidioides brasiliensis (Pb) infection, mice with homologous disruption of the IFN-gamma (GKO) or TNF-alpha receptor p55 (p55KO) were infected with the parasite. GKO and p55KO, but not wild-type (WT) mice, were unable to control the growth of yeast cells and the mice succumbed to infection by days 16 and 90 after infection, respectively. Typical inflammatory granulomas were found only in WT mice. In contrast, knockout mice presented an inflammatory infiltrate composed of a few neutrophils, mononuclear, epithelioid, and multinuclear giant cells forming incipient granulomas in GKO mice and without granuloma formation in p55KO mice. Besides, both groups of knockout mice exhibited elevated numbers of yeast forms in agreement with colony-forming unit counts in organs. Compared with WT, splenocytes from infected GKO mice cultured with the Pb F1 fraction produced lower TNF-alpha levels, whereas leukocytes from infected p55KO mice produced similar amounts of TNF-alpha but higher levels of IFN-gamma. Moreover, splenocytes from infected WT mice produced higher levels of nitric oxide (NO) resulting in a lower T-cell proliferative response to Con A than uninfected WT, or infected p55KO and GKO mice. On the contrary, the addition of IFN-gamma to splenocytes from infected GKO mice resulted in higher NO production and lower T cell proliferation. Taken together, these findings suggests that endogenous TNF-alpha, acting through the p55 receptor, and IFN-gamma mediate resistance to Pb infection and induce NO production that determines marked T cell unresponsiveness.
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