Molecular Mechanisms of Neurological Autoimmune Disorders Volume II

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 1280

Special Issue Editors


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Guest Editor
Neurology IV–Neuroimmunology and Neuromuscular Diseases Unit, Fondazione I.R.C.C.S. Istituto Neurologico Carlo Besta, 20133 Milan, Italy
Interests: autoimmunity; inflammation; innate immunity; microRNAs; myasthenia gravis; neuroimmunology; pharmacogenetics
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Neurology IV–Neuroimmunology and Neuromuscular Diseases Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Via Celoria 11, 20133 Milan, Italy
Interests: neuroimmunology, autoantibodies, neuromuscular diseases, myasthenia gravis, multiple sclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurological autoimmune disorders are a broad and heterogenous group of autoimmune diseases affecting the central (i.e., brain, spinal cord, CNS) and peripheral (i.e., peripheral nerves, neuromuscular junction, skeletal muscle, PNS) nervous systems, leading to a wide spectrum of symptoms and multifaceted clinical manifestations. They include demyelinating disorders such as multiple sclerosis (MS) and neuromyelitis optica (NMO), autoimmune encephalitis, Guillain–Barrè syndrome, and myasthenia gravis (MG). MG is widely considered a prototypic autoimmune disease, due to the well-known role of autoantibodies for neuromuscular junction proteins as a cause of the disease. The discovery of autoantibodies for neuronal or glial targets is still an open research field, which may allow for gaining a major understanding of CNS autoimmunity, with relevant clinical implications.

This Special Issue aims to increase scientific knowledge on the pathogenic mechanisms underlying autoimmunity in neurological diseases, including MS, NMO, autoimmune encephalitis, Guillain–Barrè syndrome, and MG. It will be focused on the role of autoantibodies, and on genetic and environmental (e.g., infections) risk factors associated with autoimmunity development. Original data on the contribution of neuroinflammation, as well as on central and peripheral immune system cell (e.g., innate immune system cell, T and B cell) alterations, will be collected. Manuscripts providing insights on non-coding RNAs as molecular factors implicated in immune tolerance breakdown, or clinical biomarkers for these disorders, are also welcome.

New findings on the molecular events leading to CNS and PNS autoimmune disorders will promote translational research, paving the way for the development of more specific and effective therapies for the treatment of these conditions.

Dr. Paola Cavalcante
Dr. Francesca Andreetta
Guest Editors

Manuscript Submission Information

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Keywords

  • neurological autoimmune disorders
  • multiple sclerosis
  • neuromyelitis optica
  • autoimmune encephalitis
  • Guillain–Barrè syndrome
  • myasthenia gravis
  • autoantibodies
  • neuroinflammation
  • innate and adaptive immune systems
  • non-coding RNAs

Published Papers (1 paper)

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Research

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Article
Treated and Untreated Primary Progressive Multiple Sclerosis: Walkthrough Immunological Changes of Monocytes and T Regulatory Cells
by Nina Ipavec, Maja Rogić Vidaković, Anita Markotić, Sanda Pavelin, Maja Buljubašić Šoda, Joško Šoda, Krešimir Dolić and Nikolina Režić Mužinić
Biomedicines 2024, 12(2), 464; https://doi.org/10.3390/biomedicines12020464 - 19 Feb 2024
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Abstract
The objective of this study was to investigate regulatory T cells (Tregs) and monocytes; specifically, the expression of CTLA-4 (CD152) and FOXP3+ in CD4+CD25+ Tregs and the expression of CD40+ and CD192+ monocyte subpopulations in subjects with primary progressive [...] Read more.
The objective of this study was to investigate regulatory T cells (Tregs) and monocytes; specifically, the expression of CTLA-4 (CD152) and FOXP3+ in CD4+CD25+ Tregs and the expression of CD40+ and CD192+ monocyte subpopulations in subjects with primary progressive multiple sclerosis (PPMS). Immunological analysis was conducted on peripheral blood samples collected from the 28 PPMS subjects (15 treated with ocrelizumab and 13 untreated PPMS subjects) and 10 healthy control subjects (HCs). The blood samples were incubated with antihuman CD14, CD16, CD40, and CD192 antibodies for monocytes and antihuman CD4, CD25, FOXP3, and CTLA-4 antibodies for lymphocytes. The study results showed that in comparison to HCs both ocrelizumab treated (N = 15) and untreated (N = 13) PPMS subjects had significantly increased percentages of CTLA-4+ and FOXP3+ in CD4+CD25+ Tregs. Further, ocrelizumab treated PPMS subjects, compared to the untreated ones, had significantly decreased percentages of CD192+ and CD40+ nonclassical monocytes. Increased percentages of CTLA-4+ and FOXP3+ in CD4+CD25+ Tregs in both ocrelizumab treated and untreated PPMS subjects indicates the suppressive (inhibitory) role of Tregs in abnormal immune responses in PPMS subjects. Decreased percentages of CD40+ and CD192+ non-classical CD14+CD16++ monocytes for treated compared to untreated PPMS subjects suggest a possible role for ocrelizumab in dampening CNS inflammation. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neurological Autoimmune Disorders Volume II)
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