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Pathophysiological Insights, Biomarkers and New Therapeutic Strategies in Immune-Mediated Disorders and Neurodegenerative Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 February 2026 | Viewed by 1155

Special Issue Editor


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Guest Editor
Neurology Unit, Department of Clinical and Biological Sciences, University Hospital San Luigi Gonzaga, University of Turin, 10043 Turin, Italy
Interests: multiple sclerosis; cognition; biomarkers; neuroimmunology

Special Issue Information

Dear Colleagues,

Neurodegenerative disorders are progressive and disabling diseases resulting in motor and cognitive disability, secondary to progressive neuronal loss with a high impact on quality of life. Moreover,  immune system dysregulation and inflammatory patterns have been recognized as involved in several neurodegenerative diseases, not only autoimmune and demyelinating ones. Although inflammation may not represent the only pathological mechanism of neurodegenerative processes, it could play a crucial effect on disease progression. Further improvement research is needed to unravel and clarify new pathophysiological mechanisms and therapeutic strategies for neurodegenerative and immune-mediated neurological disorders. Also, reliable diagnostic, prognostic, and predictive biomarkers would be essential to advancing precision medicine.

This Special Issue aims to highlight current knowledge regarding pathophysiological mechanisms, fluid biomarkers, and new therapeutic strategies in neurological diseases. Authors are welcome to cover all areas of clinical neurology, including neurodegenerative diseases and immune-mediated disorders of central and peripheral nervous system. Both original articles and reviews are welcome.

I look forward to receiving your contributions.

Dr. Eleonora Virgilio
Guest Editor

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Keywords

  • neurodegeneration
  • neuroimmunology
  • inflammation
  • biomarkers
  • treatment
  • pathophysiology
  • multiple sclerosis
  • myasthenia gravis
  • neurodegenerative disease

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Published Papers (1 paper)

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Review

16 pages, 487 KB  
Review
TNFR2 Agonism: Basic Science and Promising Treatment for Multiple Sclerosis and Related Diseases
by Denise L. Faustman, Miriam Davis and Willem M. Kuhtreiber
Int. J. Mol. Sci. 2025, 26(16), 7839; https://doi.org/10.3390/ijms26167839 - 14 Aug 2025
Viewed by 634
Abstract
The three pathological hallmarks of multiple sclerosis (MS) are inflammation, demyelination, and progressive neurodegeneration. None of the approved disease-modifying therapies for MS counters all three pathologies, and, more specifically, none is approved for neuroprotection. Axonal loss is the most significant contributor to chronic [...] Read more.
The three pathological hallmarks of multiple sclerosis (MS) are inflammation, demyelination, and progressive neurodegeneration. None of the approved disease-modifying therapies for MS counters all three pathologies, and, more specifically, none is approved for neuroprotection. Axonal loss is the most significant contributor to chronic and irreversible disability in MS. A tantalizing molecular target has emerged to uniquely counter all three MS pathologies: tumor necrosis factor receptor 2 (TNFR2). Agonism or activation of TNFR2 has been shown in MS models to induce immunosuppression, oligodendrocyte precursor differentiation, and neuroprotection. Further, in basic science studies stemming from the past 15 years, TNFR2 agonism is known to be a strong inducer of T-regulatory cells (Tregs). Treg cells, and especially those expressing TNFR2, are known to confer the strongest suppression per cell type. TNFR2 is even more attractive as a therapeutic target because of its restricted expression by only a handful of CNS and immune cell subsets, thereby minimizing the likelihood of systemic and other adverse effects. Recent antibody design work suggests many of the hurdles of Treg agonism may have been overcome. This review covers the current treatment landscape for MS, the basic science of TNFR2, the rationale for and evidence behind TNFR2 agonism to treat multiple sclerosis, the design of potent TNFR2 agonist antibodies, and the treatment applications for other neurological, autoimmune, or inflammatory diseases. Full article
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