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Tolerogenic Transcriptional Signatures of Steady-State and Pathogen-Induced Dendritic Cells
Dendritic cells (DCs) are key directors of tolerogenic and immunogenic immune responses. During the steady state, DCs maintain T cell tolerance to self-antigens by multiple mechanisms including inducing anergy, deletion, and Treg activity. All of these mechanisms help to prevent autoimmune diseases...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835767/ https://www.ncbi.nlm.nih.gov/pubmed/29541071 http://dx.doi.org/10.3389/fimmu.2018.00333 |
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author | Vendelova, Emilia Ashour, Diyaaeldin Blank, Patrick Erhard, Florian Saliba, Antoine-Emmanuel Kalinke, Ulrich Lutz, Manfred B. |
author_facet | Vendelova, Emilia Ashour, Diyaaeldin Blank, Patrick Erhard, Florian Saliba, Antoine-Emmanuel Kalinke, Ulrich Lutz, Manfred B. |
author_sort | Vendelova, Emilia |
collection | PubMed |
description | Dendritic cells (DCs) are key directors of tolerogenic and immunogenic immune responses. During the steady state, DCs maintain T cell tolerance to self-antigens by multiple mechanisms including inducing anergy, deletion, and Treg activity. All of these mechanisms help to prevent autoimmune diseases or other hyperreactivities. Different DC subsets contribute to pathogen recognition by expression of different subsets of pattern recognition receptors, including Toll-like receptors or C-type lectins. In addition to the triggering of immune responses in infected hosts, most pathogens have evolved mechanisms for evasion of targeted responses. One such strategy is characterized by adopting the host’s T cell tolerance mechanisms. Understanding these tolerogenic mechanisms is of utmost importance for therapeutic approaches to treat immune pathologies, tumors and infections. Transcriptional profiling has developed into a potent tool for DC subset identification. Here, we review and compile pathogen-induced tolerogenic transcriptional signatures from mRNA profiling data of currently available bacterial- or helminth-induced transcriptional signatures. We compare them with signatures of tolerogenic steady-state DC subtypes to identify common and divergent strategies of pathogen induced immune evasion. Candidate molecules are discussed in detail. Our analysis provides further insights into tolerogenic DC signatures and their exploitation by different pathogens. |
format | Online Article Text |
id | pubmed-5835767 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-58357672018-03-14 Tolerogenic Transcriptional Signatures of Steady-State and Pathogen-Induced Dendritic Cells Vendelova, Emilia Ashour, Diyaaeldin Blank, Patrick Erhard, Florian Saliba, Antoine-Emmanuel Kalinke, Ulrich Lutz, Manfred B. Front Immunol Immunology Dendritic cells (DCs) are key directors of tolerogenic and immunogenic immune responses. During the steady state, DCs maintain T cell tolerance to self-antigens by multiple mechanisms including inducing anergy, deletion, and Treg activity. All of these mechanisms help to prevent autoimmune diseases or other hyperreactivities. Different DC subsets contribute to pathogen recognition by expression of different subsets of pattern recognition receptors, including Toll-like receptors or C-type lectins. In addition to the triggering of immune responses in infected hosts, most pathogens have evolved mechanisms for evasion of targeted responses. One such strategy is characterized by adopting the host’s T cell tolerance mechanisms. Understanding these tolerogenic mechanisms is of utmost importance for therapeutic approaches to treat immune pathologies, tumors and infections. Transcriptional profiling has developed into a potent tool for DC subset identification. Here, we review and compile pathogen-induced tolerogenic transcriptional signatures from mRNA profiling data of currently available bacterial- or helminth-induced transcriptional signatures. We compare them with signatures of tolerogenic steady-state DC subtypes to identify common and divergent strategies of pathogen induced immune evasion. Candidate molecules are discussed in detail. Our analysis provides further insights into tolerogenic DC signatures and their exploitation by different pathogens. Frontiers Media S.A. 2018-02-28 /pmc/articles/PMC5835767/ /pubmed/29541071 http://dx.doi.org/10.3389/fimmu.2018.00333 Text en Copyright © 2018 Vendelova, Ashour, Blank, Erhard, Saliba, Kalinke and Lutz. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Vendelova, Emilia Ashour, Diyaaeldin Blank, Patrick Erhard, Florian Saliba, Antoine-Emmanuel Kalinke, Ulrich Lutz, Manfred B. Tolerogenic Transcriptional Signatures of Steady-State and Pathogen-Induced Dendritic Cells |
title | Tolerogenic Transcriptional Signatures of Steady-State and Pathogen-Induced Dendritic Cells |
title_full | Tolerogenic Transcriptional Signatures of Steady-State and Pathogen-Induced Dendritic Cells |
title_fullStr | Tolerogenic Transcriptional Signatures of Steady-State and Pathogen-Induced Dendritic Cells |
title_full_unstemmed | Tolerogenic Transcriptional Signatures of Steady-State and Pathogen-Induced Dendritic Cells |
title_short | Tolerogenic Transcriptional Signatures of Steady-State and Pathogen-Induced Dendritic Cells |
title_sort | tolerogenic transcriptional signatures of steady-state and pathogen-induced dendritic cells |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835767/ https://www.ncbi.nlm.nih.gov/pubmed/29541071 http://dx.doi.org/10.3389/fimmu.2018.00333 |
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