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Cells
Special Issues
Molecular and Cellular Mechanisms of Central Nervous System Autoimmunity
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Molecular and Cellular Mechanisms of Central Nervous System Autoimmunity

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 20 June 2025 | Viewed by 1159

Special Issue Editors

Prof. Dr. Refik Pul

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Guest Editor
Neurology Department, Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstr. 55, 45147 Essen, Germany
Interests: neuroimmunology; multiple sclerosis (clinical/experimental); animal models; glial cells; biomarkers in MS; neuroprotection; neuroimaging
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Christoph Kleinschnitz

E-Mail Website
Guest Editor
Neurology Department, Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstr. 55, 45147 Essen, Germany
Interests: neuroimmunology; multiple sclerosis (clinical/experimental); stroke (clinical/experimental); thromboinflammation; neuroprotection; neuroimaging
Special Issues, Collections and Topics in MDPI journals
Dr. Jelena Skuljec

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Guest Editor
Neurology Department, Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Universitätsklinikum Essen, Hufelandstr. 55, 45147 Essen, Germany
Interests: neuroimmunology; multiple sclerosis (clinical/experimental); animal models; glial cells; immune tolerance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to explore the complex relationships and interactions between the central nervous system (CNS) and immune system based on maintaining immune balance in our bodies and developing and responding to autoimmune diseases that affect these vital systems. The immune system has evolved several mechanisms to control self-reactivity, and disruptions in one or more of these mechanisms can lead to a breakdown of immune tolerance. Autoreactivity ranges from a physiological level of self-reactivity to immune-mediated organ damage. Immune-mediated CNS attacks are predominantly triggered by cell-mediated mechanisms or autoantibodies directed against neural or glial target antigens.

This dynamic interdisciplinary field represents a rapidly expanding area of translational research that could potentially improve diagnosis, prognosis, and treatment outcomes. New antibodies or targets have continued to be described in antibody-mediated CNS autoimmunity, such as antibodies specific to oligodendrocyte myelin glycoprotein. Some previously seronegative or tumefactive disease manifestations can be assigned to this new entity.

With a focus on experimental cellular biology, we welcome the submission of original research and review articles addressing the molecular and cellular events implicated in the breakdown of CNS immune tolerance; the exacerbation of inflammation, demyelination, and neurodegeneration; novel aspects of current therapeutic interventions for CNS autoimmune diseases; and the discovery of advanced strategies to prevent or treat these complex disorders.

Prof. Dr. Refik Pul
Prof. Dr. Christoph Kleinschnitz
Dr. Jelena Skuljec
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neuroimmunity
  • central nervous system
  • autoimmunity
  • immune tolerance
  • multiple sclerosis
  • antibody-mediated autoimmunity
  • cellular immunology
  • neuroinflammation

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

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Research

20 pages, 4176 KiB  
Article
Effects of Anti-CD20 Antibody Therapy on Immune Cell Dynamics in Relapsing-Remitting Multiple Sclerosis
by Alice G. Willison, Ramona Hagler, Margit Weise, Saskia Elben, Niklas Huntemann, Lars Masanneck, Steffen Pfeuffer, Stefanie Lichtenberg, Kristin S. Golombeck, Lara-Maria Preuth, Leoni Rolfes, Menekse Öztürk, Tobias Ruck, Nico Melzer, Melanie Korsen, Stephen L. Hauser, Hans-Peter Hartung, Philipp A. Lang, Marc Pawlitzki, Saskia Räuber and Sven G. Meuthadd Show full author list remove Hide full author list
Cells 2025, 14(7), 552; https://doi.org/10.3390/cells14070552 - 6 Apr 2025
Viewed by 632
Abstract
Introduction: The efficacy of anti-CD20 antibodies has significantly contributed to advancing our understanding of disease pathogenesis and improved treatment outcomes in relapsing-remitting multiple sclerosis (RRMS). A comprehensive analysis of the peripheral immune cell profile, combined with prospective clinical characterization, of RRMS patients treated [...] Read more.
Introduction: The efficacy of anti-CD20 antibodies has significantly contributed to advancing our understanding of disease pathogenesis and improved treatment outcomes in relapsing-remitting multiple sclerosis (RRMS). A comprehensive analysis of the peripheral immune cell profile, combined with prospective clinical characterization, of RRMS patients treated with ocrelizumab (OCR) or ofatumumab (OFA) was performed to further understand immune reconstitution following B-cell depletion. Methods: REBELLION-MS is a longitudinal analysis of RRMS patients treated with either OCR (n = 34) or OFA (n = 25). Analysis of B, T, natural killer (NK) and natural killer T (NKT) cells at baseline, month 1, and 12 was performed by multidimensional flow cytometry. Data were analyzed by conventional gating and unsupervised computational approaches. In parallel, different clinical parameters were longitudinally assessed. Twenty treatment-naïve age/sex-matched RRMS patients were included as the control cohort. Results: B-cell depletion by OCR and OFA resulted in significant reductions in CD20+ T and B cells as well as B-cell subsets, alongside an expansion of CD5+CD19+CD20− B cells, while also elevating exhaustion markers (CTLA-4, PD-1, TIGIT, TIM-3) across T, B, NK, and NKT cells. Additionally, regulatory T-cell (TREG) numbers increased, especially in OCR-treated patients, and reductions in double-negative (CD3+CD4−CD8−) T cells (DN T cells) were observed, with these DN T cells having higher CD20 expression compared to CD4 or CD8 positive T cells. These immune profile changes correlated with clinical parameters, suggesting pathophysiological relevance in RRMS. Conclusions: Our interim data add weight to the argumentation that the exhaustion/activation markers, notably TIGIT, may be relevant to the pathogenesis of MS. In addition, we identify a potentially interesting increase in the expression of CD5+ on B cells. Finally, we identified a population of double-negative T cells (KLRG1+HLADR+, in particular) that is associated with MS activity and decreased with CD20 depletion. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Central Nervous System Autoimmunity)
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