ArticleThe Journal of experimental medicine2015
Neutrophils are required for both the sensitization and elicitation phase of contact hypersensitivity.
Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 174 citations in OpenAlex.
- Targeting CXCR1/2 suppresses TThe journal of allergy and clinical immunology. Global · 2026Article
- Hapten-Specific Cellular Immune Responses in the Elicitation and Sensitization Phases of Murine Contact Hypersensitivity.Biomolecules · 2025Article
- Allergic Contact Dermatitis: Immunopathology and Potential Therapeutic Strategies.Journal of clinical medicine · 2025Review
- The crosstalk of monocyte-neutrophil in hair follicles regulates neutrophil transepidermal migration in contact dermatitis.Communications biology · 2025Article
- ARHGAP25: a novel player in the Pathomechanism of allergic contact hypersensitivity.Frontiers in immunology · 2025Article
- Independent risk and protective factors for oxaliplatin-induced hypersensitivity reactions: a retrospective study.Frontiers in pharmacology · 2025Article
- Cyclosporin A-loaded dissolving microneedles for dermatitis therapy: Development, characterisation and efficacy in a delayed-type hypersensitivity in vivo model.Drug delivery and translational research · 2024Article
- Bioinformatics analysis identifies WNK1 gene as a potential biomarker for cholangiocarcinoma diagnosis and immune infiltration.Journal, genetic engineering & biotechnology · 2024Article
- Neutrophils and NADPH Oxidases Are Major Contributors to Mild but Not Severe Ischemic Acute Kidney Injury in Mice.International journal of molecular sciences · 2024Article
- Article
- Proton pump inhibitor alters Th17/Treg balance and induces gut dysbiosis suppressing contact hypersensitivity reaction in mice.Frontiers in immunology · 2024Article
- Investigation of inflammatory mechanisms induced by croton oil in mouse ear.Current research in toxicology · 2024Article
- The junctional adhesion molecule-like protein (JAML) is important for the inflammatory response during contact hypersensitivity.Contact dermatitis · 2023Article
- Article
- GPR35 and mediators from platelets and mast cells in neutrophil migration and inflammation.Immunological reviews · 2023Review
- Curcumin inhibits the pruritus in mice through mast cell MrgprB2 receptor.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Neuroimmune interactions in atopic and allergic contact dermatitis.The Journal of allergy and clinical immunology · 2023Review
- Could eggshell membrane be an adjuvant for recombinant Hepatitis B vaccine?: A preliminary investigation.Future journal of pharmaceutical sciences · 2023Article
- Neutrophil depletion for early allogeneic islet survival in a methacrylic acid (MAA) copolymer-induced, vascularized subcutaneous space.Frontiers in transplantation · 2023Article
- Ethylhexadecyldimethylammonium bromide, a quaternary ammonium compound, controls inflammatory response through NRF2 pathway in a human immortalized keratinocyte cell line.Frontiers in toxicology · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Allergic contact dermatitis and its animal model, contact hypersensitivity (CHS), are T cell-mediated inflammatory skin diseases induced by contact allergens. Though numerous cellular and molecular players are known, the mechanism of chemical-induced sensitization remains poorly understood. Here, we identify neutrophils as crucial players in the sensitization phase of CHS. Genetic deficiency of neutrophils caused by myeloid-specific deletion of Mcl-1 or antibody-mediated depletion of neutrophils before sensitization abrogated the CHS response. Neutrophil deficiency reduced contact allergen-induced cytokine production, gelatinase release, and reactive oxygen species production in naive mice. Mast cell deficiency inhibited neutrophil accumulation at the site of sensitization. In turn, neutrophils were required for contact allergen-induced release of further neutrophil-attracting chemokines, migration of DCs to the draining lymph nodes, and priming of allergen-specific T cells. Lymph node cells from mice sensitized in the absence of neutrophils failed to transfer sensitization to naive recipients. Furthermore, no CHS response could be induced when neutrophils were depleted before elicitation or when normally sensitized lymph node cells were transferred to neutrophil-deficient recipients, indicating an additional role for neutrophils in the elicitation phase. Collectively, our data identify neutrophils to be critically involved in both the sensitization and elicitation phase of CHS.
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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.