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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...

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Autores principales: Lucchino, Bruno, Spinelli, Francesca Romani, Iannuccelli, Cristina, Guzzo, Maria Paola, Conti, Fabrizio, Franco, Manuela Di
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
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.
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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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