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Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies
In Spondyloarthropathies (SpA), a common group of immune-mediated diseases characterised by excessive inflammation of musculo-skeletal structures and extra-articular organs, T helper 17 (Th17) cells are widely considered the main drivers of the disease. Th17 are able to modulate their genes accordin...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8492997/ https://www.ncbi.nlm.nih.gov/pubmed/34630512 http://dx.doi.org/10.3389/fgene.2021.703242 |
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author | Simone, Davide Stingo, Alessia Ciccia, Francesco |
author_facet | Simone, Davide Stingo, Alessia Ciccia, Francesco |
author_sort | Simone, Davide |
collection | PubMed |
description | In Spondyloarthropathies (SpA), a common group of immune-mediated diseases characterised by excessive inflammation of musculo-skeletal structures and extra-articular organs, T helper 17 (Th17) cells are widely considered the main drivers of the disease. Th17 are able to modulate their genes according to the immune environment: upon differentiation, they can adopt either housekeeping, anti-bacterial gene modules or inflammatory, pathogenic functions, and only the latter would mediate immune diseases, such as SpA. Experimental work aimed at characterising Th17 heterogeneity is largely performed on murine cells, for which the in vitro conditions conferring pathogenic potential have been identified and replicated. Interestingly, Th17 recognising different microorganisms are able to acquire specific cytokine signatures. An emerging area of research associates this heterogeneity to the preferential metabolic needs of the cell. In summary, the tissue environment could be determinant for the acquisition of pathogenetic features; this is particularly important at barrier sites, such as the intestine, considered one of the key target organs in SpA, and likely a site of immunological changes that initiate the disease. In this review, we briefly summarise genetic, environmental and metabolic factors that could explain how homeostatic, anti-microbial Th17 could turn into disease-causing cells in Spondyloarthritis. |
format | Online Article Text |
id | pubmed-8492997 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-84929972021-10-07 Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies Simone, Davide Stingo, Alessia Ciccia, Francesco Front Genet Genetics In Spondyloarthropathies (SpA), a common group of immune-mediated diseases characterised by excessive inflammation of musculo-skeletal structures and extra-articular organs, T helper 17 (Th17) cells are widely considered the main drivers of the disease. Th17 are able to modulate their genes according to the immune environment: upon differentiation, they can adopt either housekeeping, anti-bacterial gene modules or inflammatory, pathogenic functions, and only the latter would mediate immune diseases, such as SpA. Experimental work aimed at characterising Th17 heterogeneity is largely performed on murine cells, for which the in vitro conditions conferring pathogenic potential have been identified and replicated. Interestingly, Th17 recognising different microorganisms are able to acquire specific cytokine signatures. An emerging area of research associates this heterogeneity to the preferential metabolic needs of the cell. In summary, the tissue environment could be determinant for the acquisition of pathogenetic features; this is particularly important at barrier sites, such as the intestine, considered one of the key target organs in SpA, and likely a site of immunological changes that initiate the disease. In this review, we briefly summarise genetic, environmental and metabolic factors that could explain how homeostatic, anti-microbial Th17 could turn into disease-causing cells in Spondyloarthritis. Frontiers Media S.A. 2021-09-22 /pmc/articles/PMC8492997/ /pubmed/34630512 http://dx.doi.org/10.3389/fgene.2021.703242 Text en Copyright © 2021 Simone, Stingo and Ciccia. https://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(s) 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 | Genetics Simone, Davide Stingo, Alessia Ciccia, Francesco Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies |
title | Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies |
title_full | Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies |
title_fullStr | Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies |
title_full_unstemmed | Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies |
title_short | Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies |
title_sort | genetic and environmental determinants of t helper 17 pathogenicity in spondyloarthropathies |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8492997/ https://www.ncbi.nlm.nih.gov/pubmed/34630512 http://dx.doi.org/10.3389/fgene.2021.703242 |
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