ArticlePLoS biology2022
The antimicrobial peptide cathelicidin drives development of experimental autoimmune encephalomyelitis in mice by affecting Th17 differentiation.
Article in PLoS biology, 2022. 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, 14 citations in OpenAlex.
- Antimicrobial proteins regulating neuroinflammation.Annals of medicine · 2026Review
- Peptidoglycan recognition proteins in the brain: Role in neuroinflammation and behavioral consequences.Histology and histopathology · 2026Review
- Citrullination of CAMP exacerbating mucosal inflammation in inflammatory bowel disease.Precision clinical medicine · 2025Article
- Cathelicidin-related antimicrobial peptide (CRAMP) is toxic during neonatal murine influenza virus infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Proteomic analysis reveals dysregulation of peripheral blood neutrophils in patients with Multiple Sclerosis.Clinical and experimental immunology · 2025Article
- The critical role of Th17 cells and IL-17A in autoimmune and inflammation-associated neurological diseases: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
- Alterations in neutrophil mRNA profiles in multiple sclerosis and identification of candidate genes for further investigation.Frontiers in neurology · 2025Article
- The Impact of Microbiota-Immunity-Hormone Interactions on Autoimmune Diseases and Infection.Biomedicines · 2024Review
- Neutrophils in Inflammatory Diseases: Unraveling the Impact of Their Derived Molecules and Heterogeneity.Cells · 2023Review
- Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is a highly prevalent demyelinating autoimmune condition; the mechanisms regulating its severity and progression are unclear. The IL-17-producing Th17 subset of T cells has been widely implicated in MS and in the mouse model, experimental autoimmune encephalomyelitis (EAE). However, the differentiation and regulation of Th17 cells during EAE remain incompletely understood. Although evidence is mounting that the antimicrobial peptide cathelicidin profoundly affects early T cell differentiation, no studies have looked at its role in longer-term T cell responses. Now, we report that cathelicidin drives severe EAE disease. It is released from neutrophils, microglia, and endothelial cells throughout disease; its interaction with T cells potentiates Th17 differentiation in lymph nodes and Th17 to exTh17 plasticity and IFN-γ production in the spinal cord. As a consequence, mice lacking cathelicidin are protected from severe EAE. In addition, we show that cathelicidin is produced by the same cell types in the active brain lesions in human MS disease. We propose that cathelicidin exposure results in highly activated, cytokine-producing T cells, which drive autoimmunity; this is a mechanism through which neutrophils amplify inflammation in the central nervous system.
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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.