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Mucosa–Environment Interactions in the Pathogenesis of Rheumatoid Arthritis
Mucosal surfaces play a central role in the pathogenesis of rheumatoid arthritis (RA). Several risk factors, such as cigarette smoking, environmental pollution, and periodontitis interact with the host at the mucosal level, triggering immune system activation. Moreover, the alteration of microbiota...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678242/ https://www.ncbi.nlm.nih.gov/pubmed/31295951 http://dx.doi.org/10.3390/cells8070700 |
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author | Lucchino, Bruno Spinelli, Francesca Romani Iannuccelli, Cristina Guzzo, Maria Paola Conti, Fabrizio Franco, Manuela Di |
author_facet | Lucchino, Bruno Spinelli, Francesca Romani Iannuccelli, Cristina Guzzo, Maria Paola Conti, Fabrizio Franco, Manuela Di |
author_sort | Lucchino, Bruno |
collection | PubMed |
description | Mucosal surfaces play a central role in the pathogenesis of rheumatoid arthritis (RA). Several risk factors, such as cigarette smoking, environmental pollution, and periodontitis interact with the host at the mucosal level, triggering immune system activation. Moreover, the alteration of microbiota homeostasis is gaining increased attention for its involvement in the disease pathogenesis, modulating the immune cell response at a local and subsequently at a systemic level. Currently, the onset of the clinical manifest arthritis is thought to be the last step of a series of pathogenic events lasting years. The positivity for anti-citrullinated protein antibodies (ACPAs) and rheumatoid factor (RF), in absence of symptoms, characterizes a preclinical phase of RA—namely systemic autoimmune phase- which is at high risk for disease progression. Several immune abnormalities, such as local ACPA production, increased T cell polarization towards a pro-inflammatory phenotype, and innate immune cell activation can be documented in at-risk subjects. Many of these abnormalities are direct consequences of the interaction between the environment and the host, which takes place at the mucosal level. The purpose of this review is to describe the humoral and cellular immune abnormalities detected in subjects at risk of RA, highlighting their origin from the mucosa–environment interaction. |
format | Online Article Text |
id | pubmed-6678242 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-66782422019-08-19 Mucosa–Environment Interactions in the Pathogenesis of Rheumatoid Arthritis Lucchino, Bruno Spinelli, Francesca Romani Iannuccelli, Cristina Guzzo, Maria Paola Conti, Fabrizio Franco, Manuela Di Cells Review Mucosal surfaces play a central role in the pathogenesis of rheumatoid arthritis (RA). Several risk factors, such as cigarette smoking, environmental pollution, and periodontitis interact with the host at the mucosal level, triggering immune system activation. Moreover, the alteration of microbiota homeostasis is gaining increased attention for its involvement in the disease pathogenesis, modulating the immune cell response at a local and subsequently at a systemic level. Currently, the onset of the clinical manifest arthritis is thought to be the last step of a series of pathogenic events lasting years. The positivity for anti-citrullinated protein antibodies (ACPAs) and rheumatoid factor (RF), in absence of symptoms, characterizes a preclinical phase of RA—namely systemic autoimmune phase- which is at high risk for disease progression. Several immune abnormalities, such as local ACPA production, increased T cell polarization towards a pro-inflammatory phenotype, and innate immune cell activation can be documented in at-risk subjects. Many of these abnormalities are direct consequences of the interaction between the environment and the host, which takes place at the mucosal level. The purpose of this review is to describe the humoral and cellular immune abnormalities detected in subjects at risk of RA, highlighting their origin from the mucosa–environment interaction. MDPI 2019-07-10 /pmc/articles/PMC6678242/ /pubmed/31295951 http://dx.doi.org/10.3390/cells8070700 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Lucchino, Bruno Spinelli, Francesca Romani Iannuccelli, Cristina Guzzo, Maria Paola Conti, Fabrizio Franco, Manuela Di Mucosa–Environment Interactions in the Pathogenesis of Rheumatoid Arthritis |
title | Mucosa–Environment Interactions in the Pathogenesis of Rheumatoid Arthritis |
title_full | Mucosa–Environment Interactions in the Pathogenesis of Rheumatoid Arthritis |
title_fullStr | Mucosa–Environment Interactions in the Pathogenesis of Rheumatoid Arthritis |
title_full_unstemmed | Mucosa–Environment Interactions in the Pathogenesis of Rheumatoid Arthritis |
title_short | Mucosa–Environment Interactions in the Pathogenesis of Rheumatoid Arthritis |
title_sort | mucosa–environment interactions in the pathogenesis of rheumatoid arthritis |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678242/ https://www.ncbi.nlm.nih.gov/pubmed/31295951 http://dx.doi.org/10.3390/cells8070700 |
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