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Cells
Special Issues
Cellular Mechanisms in Autoimmune Encephalitis: Biology and Potential Therapeutic Implications
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Cellular Mechanisms in Autoimmune Encephalitis: Biology and Potential Therapeutic Implications

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

Deadline for manuscript submissions: 31 January 2025 | Viewed by 563

Special Issue Editors

Dr. Mar Petit-Pedrol

E-Mail Website
Guest Editor
Werfen Autoimmunity, OEM Technological Center, Barcelona, Spain
Interests: autoimmunity; diagnosis; IVD
Dr. Dominique Fernandes

E-Mail Website
Guest Editor
Interdisciplinary Institute for Neuroscience, IINS-CNRS, Bordeaux, France
Interests: synaptic biology; neuropsychiatric disorders; autoimmunity

Special Issue Information

Dear Colleagues,

Neuroimmune disorders encompass a diverse spectrum of conditions characterized by inflammation of the central nervous system. In recent years, investigations into cell- and antibody-mediated neurological disorders have unveiled a multitude of factors that may trigger the onset of these conditions, such as paraneoplastic associations, infection-induced responses, or genetic predisposition. 

The aim of this Special Issue is to comprehensively explore all facets of autoimmune neurological disorders, with a particular focus on the underlying pathophysiological mechanisms and genetics, current therapeutic strategies, and emerging challenges in this field.

We cordially invite experts with an interest in this Special Issue to submit original research manuscripts and comprehensive reviews addressing any of the aforementioned themes.

Sincerely,

Dr. Mar Petit-Pedrol
Dr. Dominique Fernandes
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

  • neuroimmunology
  • pathogenesis
  • diagnosis
  • neuroimmune disorders
  • autoimmune encephalitis

Published Papers (1 paper)

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Research

20 pages, 6164 KiB  
Article
HSV-1 and Cellular miRNAs in CSF-Derived Exosomes as Diagnostically Relevant Biomarkers for Neuroinflammation
by Christian Scheiber, Hans C. Klein, Julian M. Schneider, Tanja Schulz, Karl Bechter, Hayrettin Tumani, Thomas Kapapa, Dani Flinkman, Eleanor Coffey, Duncan Ross, Maksims Čistjakovs, Zaiga Nora-Krūkle, Daria Bortolotti, Roberta Rizzo, Modra Murovska and E. Marion Schneider
Cells 2024, 13(14), 1208; https://doi.org/10.3390/cells13141208 - 17 Jul 2024
Viewed by 283
Abstract
Virus-associated chronic inflammation may contribute to autoimmunity in a number of diseases. In the brain, autoimmune encephalitis appears related to fluctuating reactivation states of neurotropic viruses. In addition, viral miRNAs and proteins can be transmitted via exosomes, which constitute novel but highly relevant [...] Read more.
Virus-associated chronic inflammation may contribute to autoimmunity in a number of diseases. In the brain, autoimmune encephalitis appears related to fluctuating reactivation states of neurotropic viruses. In addition, viral miRNAs and proteins can be transmitted via exosomes, which constitute novel but highly relevant mediators of cellular communication. The current study questioned the role of HSV-1-encoded and host-derived miRNAs in cerebrospinal fluid (CSF)-derived exosomes, enriched from stress-induced neuroinflammatory diseases, mainly subarachnoid hemorrhage (SAH), psychiatric disorders (AF and SZ), and various other neuroinflammatory diseases. The results were compared with CSF exosomes from control donors devoid of any neuroinflammatory pathology. Serology proved positive, but variable immunity against herpesviruses in the majority of patients, except controls. Selective ultrastructural examinations identified distinct, herpesvirus-like particles in CSF-derived lymphocytes and monocytes. The likely release of extracellular vesicles and exosomes was most frequently observed from CSF monocytes. The exosomes released were structurally similar to highly purified stem-cell-derived exosomes. Exosomal RNA was quantified for HSV-1-derived miR-H2-3p, miR-H3-3p, miR-H4-3p, miR-H4-5p, miR-H6-3p, miR-H27 and host-derived miR-21-5p, miR-146a-5p, miR-155-5p, and miR-138-5p and correlated with the oxidative stress chemokine IL-8 and the axonal damage marker neurofilament light chain (NfL). Replication-associated miR-H27 correlated with neuronal damage marker NfL, and cell-derived miR-155-5p correlated with oxidative stress marker IL-8. Elevated miR-138-5p targeting HSV-1 latency-associated ICP0 inversely correlated with lower HSV-1 antibodies in CSF. In summary, miR-H27 and miR-155-5p may constitute neuroinflammatory markers for delineating frequent and fluctuating HSV-1 replication and NfL-related axonal damage in addition to the oxidative stress cytokine IL-8 in the brain. Tentatively, HSV-1 remains a relevant pathogen conditioning autoimmune processes and a psychiatric clinical phenotype. Full article
(This article belongs to the Special Issue Cellular Mechanisms in Autoimmune Encephalitis: Biology and Potential Therapeutic Implications)
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