ArticleThe Journal of infectious diseases2012
CCR5 deficiency mitigates the deleterious effects of tumor necrosis factor α antagonism in murine histoplasmosis.
Article in The Journal of infectious diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Immune genes CD247 STAT1 and LCK mediate host-pathogen interactions in sporotrichosis.Scientific reports · 2025Article
- Histoplasma Capsulatum: Mechanisms for Pathogenesis.Current topics in microbiology and immunology · 2019Review
- Tumor Necrosis Factor Alpha Antagonism Reveals a Gut/Lung Axis That Amplifies Regulatory T Cells in a Pulmonary Fungal Infection.Infection and immunity · 2018Article
- Mononuclear phagocyte-mediated antifungal immunity: the role of chemotactic receptors and ligands.Cellular and molecular life sciences : CMLS · 2015Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
In murine histoplasmosis, tumor necrosis factor α (TNF-α) antagonism increases the number of regulatory T cells (Tregs) in lungs, and these cells profoundly hinder protective immunity. Because CCR5 mediates Treg homing and proliferation, we determined the outcome of antagonizing TNF-α in CCR5(-/)(-) mice infected with Histoplasma capsulatum. The absence of CCR5 attenuated the severity of infection associated with TNF-α neutralization. Infected controls given anti-TNF-α had a 10-fold increase in the number of Tregs in lungs compared with a <2-fold increase in CCR5(-/)(-) lungs. This difference was partially attributable to impaired homing in the absence of CCR5. Neutralization of TNF-α-enhanced CCR5 ligands in wild-type lungs thus promotes a gradient between lungs and the thymus. This study elucidates the interplay between TNF-α and CCR5 in histoplasmosis. The data suggest that targeting CCR5 may improve host immunity in individuals receiving TNF-α antagonists during infection.
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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.