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Alteration of T cell cytokine production in PLPp-139-151-induced EAE in SJL mice by an immunostimulatory CpG Oligonucleotide

Experimental autoimmune encephalomyelitis (EAE) is - in certain aspects - regarded as an animal model of the human CNS autoimmune disease multiple sclerosis (MS). While in EAE CNS-autoantigen-specific immunity is induced in a defined way, the initial processes leading to CNS autoimmunity in humans a...

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Autores principales: Smolianov, Vsevolod, Dehmel, Thomas, Vollmar, Patrick, Mausberg, Anne K, Kieseier, Bernd C, Hemmer, Bernhard, Hartung, Hans P, Hofstetter, Harald H
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3126729/
https://www.ncbi.nlm.nih.gov/pubmed/21624133
http://dx.doi.org/10.1186/1742-2094-8-59
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author Smolianov, Vsevolod
Dehmel, Thomas
Vollmar, Patrick
Mausberg, Anne K
Kieseier, Bernd C
Hemmer, Bernhard
Hartung, Hans P
Hofstetter, Harald H
author_facet Smolianov, Vsevolod
Dehmel, Thomas
Vollmar, Patrick
Mausberg, Anne K
Kieseier, Bernd C
Hemmer, Bernhard
Hartung, Hans P
Hofstetter, Harald H
author_sort Smolianov, Vsevolod
collection PubMed
description Experimental autoimmune encephalomyelitis (EAE) is - in certain aspects - regarded as an animal model of the human CNS autoimmune disease multiple sclerosis (MS). While in EAE CNS-autoantigen-specific immunity is induced in a defined way, the initial processes leading to CNS autoimmunity in humans are so far unknown. Despite essential restrictions, which exist regarding the interpretation of EAE data towards MS, EAE might be a useful model to study certain basic aspects of CNS autoimmunity. Studies in MS have demonstrated that established autoimmune pathology can be critically influenced by environmental factors, in particular viral and bacterial infections. To investigate this interaction, EAE as an instrument to study CNS autoimmunity under defined conditions appears to be a suitable experimental tool. For this reason, we here investigated the influence of the Toll-like-receptor (TLR) ligand CpG oligonucleotide (CpG) on already established CNS autoimmunity in murine proteolipid protein (PLP)-induced EAE in SJL mice. CpG were found to co-stimulate PLPp-specific IFN-γ production in the peripheral immune system and in the CNS. However, CpG induced Interleukin (IL)-17 production in the inflamed CNS both alone and in combination with additional PLPp stimulation. These findings might indicate a mechanism by which systemic infections and the microbial stimuli associated with them may influence already existing CNS autoimmune pathology.
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spelling pubmed-31267292011-06-30 Alteration of T cell cytokine production in PLPp-139-151-induced EAE in SJL mice by an immunostimulatory CpG Oligonucleotide Smolianov, Vsevolod Dehmel, Thomas Vollmar, Patrick Mausberg, Anne K Kieseier, Bernd C Hemmer, Bernhard Hartung, Hans P Hofstetter, Harald H J Neuroinflammation Research Experimental autoimmune encephalomyelitis (EAE) is - in certain aspects - regarded as an animal model of the human CNS autoimmune disease multiple sclerosis (MS). While in EAE CNS-autoantigen-specific immunity is induced in a defined way, the initial processes leading to CNS autoimmunity in humans are so far unknown. Despite essential restrictions, which exist regarding the interpretation of EAE data towards MS, EAE might be a useful model to study certain basic aspects of CNS autoimmunity. Studies in MS have demonstrated that established autoimmune pathology can be critically influenced by environmental factors, in particular viral and bacterial infections. To investigate this interaction, EAE as an instrument to study CNS autoimmunity under defined conditions appears to be a suitable experimental tool. For this reason, we here investigated the influence of the Toll-like-receptor (TLR) ligand CpG oligonucleotide (CpG) on already established CNS autoimmunity in murine proteolipid protein (PLP)-induced EAE in SJL mice. CpG were found to co-stimulate PLPp-specific IFN-γ production in the peripheral immune system and in the CNS. However, CpG induced Interleukin (IL)-17 production in the inflamed CNS both alone and in combination with additional PLPp stimulation. These findings might indicate a mechanism by which systemic infections and the microbial stimuli associated with them may influence already existing CNS autoimmune pathology. BioMed Central 2011-05-30 /pmc/articles/PMC3126729/ /pubmed/21624133 http://dx.doi.org/10.1186/1742-2094-8-59 Text en Copyright ©2011 Smolianov et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Smolianov, Vsevolod
Dehmel, Thomas
Vollmar, Patrick
Mausberg, Anne K
Kieseier, Bernd C
Hemmer, Bernhard
Hartung, Hans P
Hofstetter, Harald H
Alteration of T cell cytokine production in PLPp-139-151-induced EAE in SJL mice by an immunostimulatory CpG Oligonucleotide
title Alteration of T cell cytokine production in PLPp-139-151-induced EAE in SJL mice by an immunostimulatory CpG Oligonucleotide
title_full Alteration of T cell cytokine production in PLPp-139-151-induced EAE in SJL mice by an immunostimulatory CpG Oligonucleotide
title_fullStr Alteration of T cell cytokine production in PLPp-139-151-induced EAE in SJL mice by an immunostimulatory CpG Oligonucleotide
title_full_unstemmed Alteration of T cell cytokine production in PLPp-139-151-induced EAE in SJL mice by an immunostimulatory CpG Oligonucleotide
title_short Alteration of T cell cytokine production in PLPp-139-151-induced EAE in SJL mice by an immunostimulatory CpG Oligonucleotide
title_sort alteration of t cell cytokine production in plpp-139-151-induced eae in sjl mice by an immunostimulatory cpg oligonucleotide
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3126729/
https://www.ncbi.nlm.nih.gov/pubmed/21624133
http://dx.doi.org/10.1186/1742-2094-8-59
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