The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis

Genetic background, epigenetic modifications, and environmental factors trigger autoimmune response in rheumatoid arthritis (RA). Several pathogenic infections have been related to the onset of RA and may cause an inadequate immunological tolerance towards critical self-antigens leading to chronic j...

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Main Authors: Raúl Villanueva-Romero, Irene Gutiérrez-Cañas, Mar Carrión, Selene Pérez-García, Iria V. Seoane, Carmen Martínez, Rosa P. Gomariz, Yasmina Juarranz
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2018/6043710
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author Raúl Villanueva-Romero
Irene Gutiérrez-Cañas
Mar Carrión
Selene Pérez-García
Iria V. Seoane
Carmen Martínez
Rosa P. Gomariz
Yasmina Juarranz
author_facet Raúl Villanueva-Romero
Irene Gutiérrez-Cañas
Mar Carrión
Selene Pérez-García
Iria V. Seoane
Carmen Martínez
Rosa P. Gomariz
Yasmina Juarranz
author_sort Raúl Villanueva-Romero
collection DOAJ
description Genetic background, epigenetic modifications, and environmental factors trigger autoimmune response in rheumatoid arthritis (RA). Several pathogenic infections have been related to the onset of RA and may cause an inadequate immunological tolerance towards critical self-antigens leading to chronic joint inflammation and an imbalance between different T helper (Th) subsets. Vasoactive intestinal peptide (VIP) is a mediator that modulates all the stages comprised between the arrival of pathogens and Th cell differentiation in RA through its known anti-inflammatory and immunomodulatory actions. This “neuroimmunopeptide” modulates the pathogenic activity of diverse cell subpopulations involved in RA as lymphocytes, fibroblast-like synoviocytes (FLS), or macrophages. In addition, VIP decreases the expression of pattern recognition receptor (PRR) such as toll-like receptors (TLRs) in FLS from RA patients. These receptors act as sensors of pathogen-associated molecular pattern (PAMP) and damage-associated molecular pattern (DAMP) connecting the innate and adaptive immune system. Moreover, VIP modulates the imbalance between Th subsets in RA, decreasing pathogenic Th1 and Th17 subsets and favoring Th2 or Treg profile during the differentiation/polarization of naïve or memory Th cells. Finally, VIP regulates the plasticity between theses subsets. In this review, we provide an overview of VIP effects on the aforementioned features of RA pathology.
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spelling doaj-art-62fc130d142e4a6e8e59e27c01e6a4712025-08-20T02:35:16ZengWileyJournal of Immunology Research2314-88612314-71562018-01-01201810.1155/2018/60437106043710The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid ArthritisRaúl Villanueva-Romero0Irene Gutiérrez-Cañas1Mar Carrión2Selene Pérez-García3Iria V. Seoane4Carmen Martínez5Rosa P. Gomariz6Yasmina Juarranz7Departamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, SpainDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, SpainDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, SpainDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, SpainDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, SpainDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, SpainDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, SpainDepartamento de Biología Celular, Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Universidad Complutense de Madrid, Madrid, SpainGenetic background, epigenetic modifications, and environmental factors trigger autoimmune response in rheumatoid arthritis (RA). Several pathogenic infections have been related to the onset of RA and may cause an inadequate immunological tolerance towards critical self-antigens leading to chronic joint inflammation and an imbalance between different T helper (Th) subsets. Vasoactive intestinal peptide (VIP) is a mediator that modulates all the stages comprised between the arrival of pathogens and Th cell differentiation in RA through its known anti-inflammatory and immunomodulatory actions. This “neuroimmunopeptide” modulates the pathogenic activity of diverse cell subpopulations involved in RA as lymphocytes, fibroblast-like synoviocytes (FLS), or macrophages. In addition, VIP decreases the expression of pattern recognition receptor (PRR) such as toll-like receptors (TLRs) in FLS from RA patients. These receptors act as sensors of pathogen-associated molecular pattern (PAMP) and damage-associated molecular pattern (DAMP) connecting the innate and adaptive immune system. Moreover, VIP modulates the imbalance between Th subsets in RA, decreasing pathogenic Th1 and Th17 subsets and favoring Th2 or Treg profile during the differentiation/polarization of naïve or memory Th cells. Finally, VIP regulates the plasticity between theses subsets. In this review, we provide an overview of VIP effects on the aforementioned features of RA pathology.http://dx.doi.org/10.1155/2018/6043710
spellingShingle Raúl Villanueva-Romero
Irene Gutiérrez-Cañas
Mar Carrión
Selene Pérez-García
Iria V. Seoane
Carmen Martínez
Rosa P. Gomariz
Yasmina Juarranz
The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis
Journal of Immunology Research
title The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis
title_full The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis
title_fullStr The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis
title_full_unstemmed The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis
title_short The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis
title_sort anti inflammatory mediator vasoactive intestinal peptide modulates the differentiation and function of th subsets in rheumatoid arthritis
url http://dx.doi.org/10.1155/2018/6043710
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