ArticleThe Journal of experimental medicine1997
Targeted disruption of the chemokine eotaxin partially reduces antigen-induced tissue eosinophilia.
Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 527 citations in OpenAlex.
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- Leptin augments IL-13-induced airway eotaxins and submucosal eosinophilia in obesity-associated asthma.The Journal of allergy and clinical immunology · 2025Article
- Synchronized development of thymic eosinophils and thymocytes.International immunology · 2024Article
- Fentanyl Overdose Causes Prolonged Cardiopulmonary Dysregulation in Male SKH1 Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- CCR3-dependent eosinophil recruitment is regulated by sialyltransferase ST3Gal-IV.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Trans-activation of eotaxin-1 by Brg1 contributes to liver regeneration.Cell death & disease · 2022Article
- Role of IL-18-transformed CD274-expressing eosinophils in promoting airway obstruction in experimental asthma.Allergy · 2022Article
- Recent advances of eosinophils and its correlated diseases.Frontiers in public health · 2022Review
- Eosinophils in filarial infections: Inducers of protection or pathology?Frontiers in immunology · 2022Review
- Review
- Role of Eosinophils in Intestinal Inflammation and Fibrosis in Inflammatory Bowel Disease: An Overlooked Villain?Frontiers in immunology · 2021Review
- Bioinformatic analysis of eosinophil activity and its implications for model and target species.Parasitology · 2020Review
- Intestinal overexpression of IL-18 promotes eosinophils-mediated allergic disorders.Immunology · 2019Article
- Trib1 regulates eosinophil lineage commitment and identity by restraining the neutrophil program.Blood · 2019Article
- Intestinal overexpression of interleukin (IL)-15 promotes tissue eosinophilia and goblet cell hyperplasia.Immunology and cell biology · 2018Article
- Chi3l3: a potential key orchestrator of eosinophil recruitment in meningitis induced by Angiostrongylus cantonensis.Journal of neuroinflammation · 2018Article
- OK-432 Acts as Adjuvant to Modulate T Helper 2 Inflammatory Responses in a Murine Model of Asthma.Journal of immunology research · 2018Article
57 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chemokines are a large group of chemotactic cytokines that regulate leukocyte trafficking and have recently been shown to inhibit human immunodeficiency virus entry into cells. Eotaxin is a C-C chemokine implicated in the recruitment of eosinophils in a variety of inflammatory disorders and, unlike all other eosinophil chemoattractants, is eosinophil specific. However, given the large number of chemoattractants that have activities on eosinophils, it is unclear whether eotaxin has an important role in vivo. Furthermore, it remains unclear why there is constitutive expression of eotaxin in healthy states in the absence of eosinophilic inflammation. To begin to determine the significance of eotaxin at baseline and during eosinophil-mediated disease processes, we have used targeted gene disruption to generate mice that are deficient in eotaxin. Such mice demonstrate that eotaxin enhances the magnitude of the early (but not late) eosinophil recruitment after antigen challenge in models of asthma and stromal keratitis. Surprisingly, a role for eotaxin in regulating the constitutive number of eosinophils in the peripheral circulation is also demonstrated. These results indicate a contributory role for eotaxin in the generation of peripheral blood and antigen-induced tissue eosinophilia.
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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.