ArticleFrontiers in immunology2024
A peptide mimic of SOCS1 modulates equine peripheral immune cells
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- STAT Signaling in Metabolic Disorders: From Molecular Mechanisms to Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- Potential Ferroptosis-Related Genes and Immune Infiltration in Form-Deprivation Myopia: An Integrative Bioinformatics and in vitro Validation Study.International journal of general medicine · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Introduction: Recurrent uveitis (RU), an autoimmune disease, is a leading cause of ocular detriment in humans and horses. Equine and human RU share many similarities including spontaneous disease and aberrant cytokine signaling. Reduced levels of SOCS1, a critical regulator of cytokine signaling, is associated with several autoimmune diseases. Topical administration of SOCS1-KIR, a peptide mimic of SOCS1, was previously correlated to reduced ocular pathologies within ERU patients. Methods: To further assess the translational potential of a SOCS1 mimetic to treat RU, we assessed peptide-mediated modulation of immune functions Results: Following SOCS1-KIR pretreatment, cell proliferation significantly decreased in control, but not ERU-derived PBMCs. Despite differential regulation of cellular proliferation, SOCS1-KIR significantly reduced TNFα and IL-10 secretion in PHA-stimulated control and ERU equine PBMC. SOCS1-KIR increased PBMC secretion of IL-8. Topically administered SOCS1-KIR was well tolerated. Although SOCS1-KIR was undetectable within the eye, topically treated equine eyes had significant reductions in TNFα and IL-10. Interestingly, we found that while SOCS1-KIR treatment reduced TNFα and IL-10 production in healthy and ERU PBMC, SOCS1-KIR differentially modulated proliferation, IP-10 production, and RANTES within these two groups suggesting possible differences in cell types or activation status. Discussion: Topical administration of a SOCS1 peptide mimic is safe to the equine eye and reduces ERU associated cytokines IL-10 and TNFα serving as potential biomarkers of drug efficacy in a future clinical trial.
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Registered trials
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