ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Carbonic anhydrase IV is expressed on IL-5-activated murine eosinophils.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 21 citations in OpenAlex.
- Proteomic characterization ofVirulence · 2025Article
- Investigating the Anti-Inflammatory Potential of SLC-0111: A Carbonic Anhydrase Inhibitor Targeting Cyclooxygenase-Mediated Inflammatory Pathways in a Carrageenan-Induced Rat Model.Journal of biochemical and molecular toxicology · 2025Article
- Identification of diagnostic biomarkers of and immune cell infiltration analysis in bovine respiratory disease.Frontiers in veterinary science · 2025Article
- Advancing toward a unified eosinophil signature from transcriptional profiling.Journal of leukocyte biology · 2024Review
- Review
- Eosinophils promote effector functions of lung group 2 innate lymphoid cells in allergic airway inflammation in mice.The Journal of allergy and clinical immunology · 2023Article
- Single-cell RNA Sequencing Uncovered the Involvement of an Endothelial Subset in Neutrophil Recruitment in Chemically Induced Rat Pulmonary Inflammation.International journal of medical sciences · 2022Article
- Carbonic Anhydrase Inhibition Ameliorates Inflammation and Experimental Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2019Article
- Review and Meta-Analyses of TAAR1 Expression in the Immune System and Cancers.Frontiers in pharmacology · 2018Article
- Breed and adaptive response modulate bovine peripheral blood cells' transcriptome.Journal of animal science and biotechnology · 2017Article
- Carbonic anhydrase enzymes regulate mast cell-mediated inflammation.The Journal of experimental medicine · 2016Article
- Profiles of microRNA networks in intestinal epithelial cells in a mouse model of colitis.Scientific reports · 2015Article
- IL-1β in eosinophil-mediated small intestinal homeostasis and IgA production.Mucosal immunology · 2015Article
- An Exploration of Molecular Correlates Relevant to Radiation Combined Skin-Burn Trauma.PloS one · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Eosinophilia and its cellular activation are hallmark features of asthma, as well as other allergic/Th2 disorders, yet there are few, if any, reliable surface markers of eosinophil activation. We have used a FACS-based genome-wide screening system to identify transcriptional alterations in murine lung eosinophils recruited and activated by pulmonary allergen exposure. Using a relatively stringent screen with false-positive correction, we identified 82 candidate genes that could serve as eosinophil activation markers and/or pathogenic effector markers in asthma. Carbonic anhydrase IV (Car4) was a top dysregulated gene with 36-fold induction in allergen-elicited pulmonary eosinophils, which was validated by quantitative PCR, immunohistochemistry, and flow cytometry. Eosinophil CAR4 expression was kinetically regulated by IL-5, but not IL-13. IL-5 was both necessary and sufficient for induction of eosinophil CAR4. Although CAR4-deficient mice did not have a defect in eosinophil recruitment to the lung, nor a change in eosinophil pH-buffering capacity, allergen-challenged chimeric mice that contained Car4(-/-) hematopoietic cells aberrantly expressed a series of genes enriched in biological processes involved in epithelial differentiation, keratinization, and anion exchange. In conclusion, we have determined that eosinophils express CAR4 following IL-5 or allergen exposure, and that CAR4 is involved in regulating the lung transcriptome associated with allergic airway inflammation; therefore, CAR4 has potential value for diagnosing and monitoring eosinophilic responses.
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Registered trials
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