A Novel Cytokine-Derived Peptide as a Therapeutic Modulator in Multiple Sclerosis 9158

Abstract Description Multiple sclerosis (MS) is a chronic autoimmune disease caused by demyelination of myelin in the central nervous system (CNS). The exact cause of MS remains unclear, but it is thought to involve multiple factors. Unlike other diseases, MS is driven by interactions between the immune and nervous systems, where various cells and factors contribute to the disease’s development and progression. This complexity makes it challenging to develop effective treatments for MS. KINE-PD-28 is a cytokine-derived peptide that increases the activity of Treg cells, well-known modulators of the immune system that suppress excessive or inappropriate immune responses. Our previous studies have demonstrated the therapeutic potential of KINE-PD-28 by showing that Treg cells enhanced by this peptide effectively contribute to the improvement of CIDP (Chronic Inflammatory Demyelinating Polyneuropathy), a peripheral demyelinating disease. Given that MS and CIDP share similarities in etiology, these results suggest that KINE-PD-28 could also be effective in treating MS. To investigate KINE-PD-28’s effect on MS, we utilized the EAE mouse model, which replicates key features of MS, including inflammation, demyelination, and neurodegeneration. Our results show the potential of KINE-PD-28 as a therapeutic agent for regulating MS pathology by modulating immune responses. This presents a new approach to MS drug development, providing insight into a critical unmet need in the current MS clinical area. Topic Categories Therapeutic Approaches to Autoimmunity (THER)

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Publication Details

Journal
The Journal of Immunology
Published
2025-11-01
DOI
https://doi.org/10.1093/jimmun/vkaf283.2599
Primary Topic
Multiple Sclerosis Research Studies
Type
article
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article

A Novel Cytokine-Derived Peptide as a Therapeutic Modulator in Multiple Sclerosis 9158

Changkyu Gu, Myung‐Ju Ahn, Soochul Park, Hyeonki Kim et al.
The Journal of Immunology
Multiple Sclerosis Research Studies
article

A Novel Cytokine-Derived Peptide as a Therapeutic Modulator in Multiple Sclerosis 9158

Changkyu Gu, Myung‐Ju Ahn, Soochul Park, Hyeonki Kim, Seul Hye Ryu
article en

Abstract

Abstract Description Multiple sclerosis (MS) is a chronic autoimmune disease caused by demyelination of myelin in the central nervous system (CNS). The exact cause of MS remains unclear, but it is thought to involve multiple factors. Unlike other diseases, MS is driven by interactions between the immune and nervous systems, where various cells and factors contribute to the disease’s development and progression. This complexity makes it challenging to develop effective treatments for MS. KINE-PD-28 is a cytokine-derived peptide that increases the activity of Treg cells, well-known modulators of the immune system that suppress excessive or inappropriate immune responses. Our previous studies have demonstrated the therapeutic potential of KINE-PD-28 by showing that Treg cells enhanced by this peptide effectively contribute to the improvement of CIDP (Chronic Inflammatory Demyelinating Polyneuropathy), a peripheral demyelinating disease. Given that MS and CIDP share similarities in etiology, these results suggest that KINE-PD-28 could also be effective in treating MS. To investigate KINE-PD-28’s effect on MS, we utilized the EAE mouse model, which replicates key features of MS, including inflammation, demyelination, and neurodegeneration. Our results show the potential of KINE-PD-28 as a therapeutic agent for regulating MS pathology by modulating immune responses. This presents a new approach to MS drug development, providing insight into a critical unmet need in the current MS clinical area. Topic Categories Therapeutic Approaches to Autoimmunity (THER)

The Journal of ImmunologyVol. 214(Supplement_1)
Openalex Percentile: Top 51%
Multiple Sclerosis Research Studies
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A Novel Cytokine-Derived Peptide as a Therapeutic Modulator in Multiple Sclerosis 9158 — Changkyu Gu, Myung‐Ju Ahn, et al. · The Journal of Immunology (2025) | TGRS Research Map | TGRS