ReviewDermatitis : contact, atopic, occupational, drug
Chemokine Signaling in Allergic Contact Dermatitis: Toward Targeted Therapies.
Review in Dermatitis : contact, atopic, occupational, drug. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Evasins: Biology and Therapeutic Potential of Broad-Spectrum Chemokine Inhibitors.Basic & clinical pharmacology & toxicology · 2026Review
- Dietary allergen promotes sex-specific leukocyte trafficking and alters the brain immune cell populations in subclinically sensitized mice.Brain, behavior, and immunity · 2026Article
- CCL7-CCR3 signaling mediates olfactory dysfunction in a mouse model of allergic rhinitis.Frontiers in immunology · 2026Article
- Allergic Contact Dermatitis: Immunopathology and Potential Therapeutic Strategies.Journal of clinical medicine · 2025Review
- Anti-Biofilm Properties of Cell-Free Supernatant fromMicroorganisms · 2025Article
- Systemic Immune Factors and Risk of Allergic Contact Dermatitis: A Bidirectional Mendelian Randomization Study.International journal of molecular sciences · 2024Article
- The Involvement of Cysteine-X-Cysteine Motif Chemokine Receptors in Skin Homeostasis and the Pathogenesis of Allergic Contact Dermatitis and Psoriasis.International journal of molecular sciences · 2024Review
- Topical Microemulsions: Skin Irritation Potential and Anti-Inflammatory Effects of Herbal Substances.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Phosphorylation barcodes direct biased chemokine signaling at CXCR3.Cell chemical biology · 2023Article
- 7-Methoxyisoflavone ameliorates atopic dermatitis symptoms by regulating multiple signaling pathways and reducing chemokine production.Scientific reports · 2022Article
- Contact dermatitis.Nature reviews. Disease primers · 2021Review
- CX3CR1 Deficiency Attenuates DNFB-Induced Contact Hypersensitivity Through Skewed Polarization Towards M2 Phenotype in Macrophages.International journal of molecular sciences · 2020Article
- Nivolumab-induced contact dermatitis in a patient with advanced lung cancer.Respiratory medicine case reports · 2020Article
- The Effect of Transplantation of Cultured Autologous Melanocytes on CXCL9, CXCL10 and CXCL11 Expressions in Vitiligo.Indian journal of dermatologyArticle
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Allergic contact dermatitis (ACD) is a common skin disease that results in significant cost and morbidity. Despite its high prevalence, therapeutic options are limited. Allergic contact dermatitis is regulated primarily by T cells within the adaptive immune system, but also by natural killer and innate lymphoid cells within the innate immune system. The chemokine receptor system, consisting of chemokine peptides and chemokine G protein-coupled receptors, is a critical regulator of inflammatory processes such as ACD. Specific chemokine signaling pathways are selectively up-regulated in ACD, most prominently CXCR3 and its endogenous chemokines CXCL9, CXCL10, and CXCL11. Recent research demonstrates that these 3 chemokines are not redundant and indeed activate distinct intracellular signaling profiles such as those activated by heterotrimeric G proteins and β-arrestin adapter proteins. Such differential signaling provides an attractive therapeutic target for novel therapies for ACD and other inflammatory diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.