ArticleImmunity, inflammation and disease2014
The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice.
Article in Immunity, inflammation and disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- NETosis in hypersensitivity disorders.Molecular biology reports · 2025Review
- Development and optimization of hydrogel-forming microneedles fabricated with 3d-printed molds for enhanced dermal diclofenac sodium delivery: a comprehensive in vitro, ex vivo, and in vivo study.Drug delivery and translational research · 2025Article
- Neutrophil inhibition improves acute inflammation in a murine model of viral myocarditis.Cardiovascular research · 2023Article
- I've looked at gut from both sides now: Gastrointestinal tract involvement in the pathogenesis of SARS-CoV-2 and HIV/SIV infections.Frontiers in immunology · 2022Review
- IL-36 receptor antagonist deficiency resulted in delayed wound healing due to excessive recruitment of immune cells.Scientific reports · 2020Article
- A mechanistic and empirical review of antcins, a new class of phytosterols of formosan fungi origin.Journal of food and drug analysis · 2020Review
- Neutrophil α-defensins promote thrombosis in vivo by altering fibrin formation, structure, and stability.Blood · 2019Article
- Nrf2 Involvement in Chemical-Induced Skin Innate Immunity.Frontiers in immunology · 2019Review
- Anti-colony-stimulating factor therapies for inflammatory and autoimmune diseases.Nature reviews. Drug discovery · 2016Review
- Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils are thought to play an important role during contact hypersensitivity (CHS) in mice, a notion which is supported by studies in which neutrophils are depleted by monoclonal antibodies (mAb). Here, we show that administration of the commonly used anti-mouse Ly6G/C mAb (clone RB6.8C5) leads to depletion of not only neutrophils but also a population of monocytes and macrophages. In contrast, depletion using a Ly6G-specific mAb (clone 1A8) only leads to depletion of neutrophils. We demonstrate that the anti-Ly6G/C mAb suppresses the inflammatory response to a higher extent than the anti-Ly6G mAb suggesting that the impact of neutrophil-depletion in the CHS model may have been overstated when based on protocols using the anti-Ly6G/C mAb. Still, the role of neutrophils in CHS is substantiated as we demonstrate that G-CSF is an important regulator of neutrophil mobilization and effector function in CHS. Indeed, G-CSF was detectable both in the inflamed tissue and in serum during the immune response and we show that blocking G-CSF results in a reduced number of neutrophils in the blood and an attenuation of the ear-swelling response in the tissue. In conclusion, this study supports that neutrophils are important drivers of inflammation in the DNFB-induced CHS model and shows that G-CSF is a significant factor in mobilizing neutrophils during the response.
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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.