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Dysbiosis May Trigger Autoimmune Diseases via Inappropriate Post-Translational Modification of Host Proteins

The gut ecosystem with myriads of microorganisms and the high concentration of immune system cells can be considered as a separate organ on its own. The balanced interaction between the host and microbial cells has been shaped during the long co-evolutionary process. In dysbiotic conditions, however...

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Detalles Bibliográficos
Autores principales: Lerner, Aaron, Aminov, Rustam, Matthias, Torsten
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4742538/
https://www.ncbi.nlm.nih.gov/pubmed/26903965
http://dx.doi.org/10.3389/fmicb.2016.00084
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author Lerner, Aaron
Aminov, Rustam
Matthias, Torsten
author_facet Lerner, Aaron
Aminov, Rustam
Matthias, Torsten
author_sort Lerner, Aaron
collection PubMed
description The gut ecosystem with myriads of microorganisms and the high concentration of immune system cells can be considered as a separate organ on its own. The balanced interaction between the host and microbial cells has been shaped during the long co-evolutionary process. In dysbiotic conditions, however, this balance is compromised and results in abnormal interaction between the host and microbiota. It is hypothesize here that the changed spectrum of microbial enzymes involved in post-translational modification of proteins (PTMP) may contribute to the aberrant modification of host proteins thus generating autoimmune responses by the host, resulting in autoimmune diseases.
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spelling pubmed-47425382016-02-22 Dysbiosis May Trigger Autoimmune Diseases via Inappropriate Post-Translational Modification of Host Proteins Lerner, Aaron Aminov, Rustam Matthias, Torsten Front Microbiol Immunology The gut ecosystem with myriads of microorganisms and the high concentration of immune system cells can be considered as a separate organ on its own. The balanced interaction between the host and microbial cells has been shaped during the long co-evolutionary process. In dysbiotic conditions, however, this balance is compromised and results in abnormal interaction between the host and microbiota. It is hypothesize here that the changed spectrum of microbial enzymes involved in post-translational modification of proteins (PTMP) may contribute to the aberrant modification of host proteins thus generating autoimmune responses by the host, resulting in autoimmune diseases. Frontiers Media S.A. 2016-02-05 /pmc/articles/PMC4742538/ /pubmed/26903965 http://dx.doi.org/10.3389/fmicb.2016.00084 Text en Copyright © 2016 Lerner, Aminov and Matthias. 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) or licensor 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
Lerner, Aaron
Aminov, Rustam
Matthias, Torsten
Dysbiosis May Trigger Autoimmune Diseases via Inappropriate Post-Translational Modification of Host Proteins
title Dysbiosis May Trigger Autoimmune Diseases via Inappropriate Post-Translational Modification of Host Proteins
title_full Dysbiosis May Trigger Autoimmune Diseases via Inappropriate Post-Translational Modification of Host Proteins
title_fullStr Dysbiosis May Trigger Autoimmune Diseases via Inappropriate Post-Translational Modification of Host Proteins
title_full_unstemmed Dysbiosis May Trigger Autoimmune Diseases via Inappropriate Post-Translational Modification of Host Proteins
title_short Dysbiosis May Trigger Autoimmune Diseases via Inappropriate Post-Translational Modification of Host Proteins
title_sort dysbiosis may trigger autoimmune diseases via inappropriate post-translational modification of host proteins
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4742538/
https://www.ncbi.nlm.nih.gov/pubmed/26903965
http://dx.doi.org/10.3389/fmicb.2016.00084
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