ArticleNature communications2021
The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 136 citations in OpenAlex.
- Cholinergic Signaling Attenuates Pro-Inflammatory Interleukin-8 Response in Colonic Epithelial Cells.Frontiers in immunology · 2021Trial
- Forensic application of CAMP expression for the determination of wound vitality in human compressed neck skin.International journal of legal medicine · 2026Article
- Antimicrobial Peptide BSN-37 Enhances Macrophage Immune Activation Through the circBptf-Rbm14-Mediated Regulatory Axis.Probiotics and antimicrobial proteins · 2026Article
- Impact of cathelicidin cleavage by SpeB onbioRxiv : the preprint server for biology · 2026Article
- Regenerative Microbiology: Harnessing Bacterial Antagonism and Spatiotemporal Signaling for Diabetic Wound Repair.Smart medicine · 2026Review
- Tryptophan Metabolism and Aryl-Hydrocarbon Receptor Agonists in the Gut Microbiome of People With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.MicrobiologyOpen · 2026Article
- A protease-sensing circuit links neutrophil inflammation to virulence regulation inbioRxiv : the preprint server for biology · 2026Article
- Aggregation-State Dynamics Drive Double Cooperativity Between Antimicrobial Peptides LL-37 and HNP1.Angewandte Chemie (International ed. in English) · 2026Article
- IL10R Inhibition Induces Neutrophil Tumoricidal Activity.Cancer immunology research · 2026Article
- Rosacea scleritis and sclero-uveitis; under recognised and over treated.Journal of ophthalmic inflammation and infection · 2026Review
- Stevioside curbs Streptococcus pneumoniae infection via inhibiting capsule biosynthesis.Communications biology · 2026Article
- The association between atopic dermatitis and rosacea: a comprehensive review from comorbidities to pathogenic mechanisms.Frontiers in immunology · 2026Review
- Neutrophil-T cell cross talk in noninfectious liver diseases.American journal of physiology. Gastrointestinal and liver physiology · 2026Review
- Extended-Spectrum β-Lactamase-ProducingAntibiotics (Basel, Switzerland) · 2025Review
- Neutrophil extracellular traps aggravate periodontitis by disturbing regulatory T-cell differentiation.Genes and immunity · 2025Article
- Cannabidiol as a therapeutic agent for rosacea through simultaneous inhibition of multiple inflammatory pathways.BMB reports · 2025Article
- Recent Advances in the Immunopathology of Axial Spondyloarthritis: with and without HLA-B27.Current rheumatology reports · 2025Review
- Antimicrobial Peptides in Wound Healing and Skin Regeneration: Dual Roles in Immunity and Microbial Defense.International journal of molecular sciences · 2025Review
- Remote Ischemic Post-conditioning Reduces Cognitive Impairment in Rats Following Subarachnoid Hemorrhage: Possible Involvement in STAT3/STAT5 Phosphorylation and Th17/Treg Cell Homeostasis.Translational stroke research · 2025Article
- LL-37 and citrullinated-LL-37 modulate IL-17A/F-mediated responses and selectively suppress Lipocalin-2 in bronchial epithelial cells.Journal of inflammation (London, England) · 2025Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The host defence peptide cathelicidin (LL-37 in humans, mCRAMP in mice) is released from neutrophils by de-granulation, NETosis and necrotic death; it has potent anti-pathogen activity as well as being a broad immunomodulator. Here we report that cathelicidin is a powerful Th17 potentiator which enhances aryl hydrocarbon receptor (AHR) and RORγt expression, in a TGF-β1-dependent manner. In the presence of TGF-β1, cathelicidin enhanced SMAD2/3 and STAT3 phosphorylation, and profoundly suppressed IL-2 and T-bet, directing T cells away from Th1 and into a Th17 phenotype. Strikingly, Th17, but not Th1, cells were protected from apoptosis by cathelicidin. We show that cathelicidin is released by neutrophils in mouse lymph nodes and that cathelicidin-deficient mice display suppressed Th17 responses during inflammation, but not at steady state. We propose that the neutrophil cathelicidin is required for maximal Th17 differentiation, and that this is one method by which early neutrophilia directs subsequent adaptive immune responses.
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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.