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The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis
Autoimmune encephalitis (AE) is an inflammatory brain disease which is frequently associated with antibodies (Abs) against cell-surface, synaptic or intracellular neuronal proteins. There is increasing evidence that dendritic cells (DCs) are implicated as key modulators in keeping the balance betwee...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8573920/ https://www.ncbi.nlm.nih.gov/pubmed/34749759 http://dx.doi.org/10.1186/s12974-021-02310-z |
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author | Ismail, Fatme Seval Meuth, Sven G. Melzer, Nico |
author_facet | Ismail, Fatme Seval Meuth, Sven G. Melzer, Nico |
author_sort | Ismail, Fatme Seval |
collection | PubMed |
description | Autoimmune encephalitis (AE) is an inflammatory brain disease which is frequently associated with antibodies (Abs) against cell-surface, synaptic or intracellular neuronal proteins. There is increasing evidence that dendritic cells (DCs) are implicated as key modulators in keeping the balance between immune response and tolerance in the CNS. Migratory features of DCs to and from the brain are linked to initiating and maintaining of neuroinflammation. Genetic polymorphisms together with other triggers such as systemic or cerebral viral infection, or systemic malignancies could contribute to the dysbalance of “regulatory” and “encephalitogenic” DCs with subsequent dysregulated T and B cell reactions in AE. Novel in vivo models with implantation of mature DCs containing neuronal antigens could help to study the pathogenesis and perhaps to understand the origin of AE. Investigations of DCs in human blood, lymphoid tissues, CSF, and brain parenchyma of patients with AE are necessary to deepen our knowledge about the complex interactions between DCs, T and B cells during neuroinflammation in AE. This can support developing new therapy strategies. |
format | Online Article Text |
id | pubmed-8573920 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-85739202021-11-08 The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis Ismail, Fatme Seval Meuth, Sven G. Melzer, Nico J Neuroinflammation Hypothesis Autoimmune encephalitis (AE) is an inflammatory brain disease which is frequently associated with antibodies (Abs) against cell-surface, synaptic or intracellular neuronal proteins. There is increasing evidence that dendritic cells (DCs) are implicated as key modulators in keeping the balance between immune response and tolerance in the CNS. Migratory features of DCs to and from the brain are linked to initiating and maintaining of neuroinflammation. Genetic polymorphisms together with other triggers such as systemic or cerebral viral infection, or systemic malignancies could contribute to the dysbalance of “regulatory” and “encephalitogenic” DCs with subsequent dysregulated T and B cell reactions in AE. Novel in vivo models with implantation of mature DCs containing neuronal antigens could help to study the pathogenesis and perhaps to understand the origin of AE. Investigations of DCs in human blood, lymphoid tissues, CSF, and brain parenchyma of patients with AE are necessary to deepen our knowledge about the complex interactions between DCs, T and B cells during neuroinflammation in AE. This can support developing new therapy strategies. BioMed Central 2021-11-08 /pmc/articles/PMC8573920/ /pubmed/34749759 http://dx.doi.org/10.1186/s12974-021-02310-z Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Hypothesis Ismail, Fatme Seval Meuth, Sven G. Melzer, Nico The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis |
title | The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis |
title_full | The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis |
title_fullStr | The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis |
title_full_unstemmed | The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis |
title_short | The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis |
title_sort | role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis |
topic | Hypothesis |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8573920/ https://www.ncbi.nlm.nih.gov/pubmed/34749759 http://dx.doi.org/10.1186/s12974-021-02310-z |
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