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.

Mucosa-Environment Interactions in the Pathogenesis of Rheumatoid Arthritis / Lucchino, Bruno; Spinelli, Francesca Romani; Iannuccelli, Cristina; Guzzo, Maria Paola; Conti, Fabrizio; Di Franco, Manuela. - In: CELLS. - ISSN 2073-4409. - 8:7(2019), p. 700. [10.3390/cells8070700]

Mucosa-Environment Interactions in the Pathogenesis of Rheumatoid Arthritis

Lucchino, Bruno;Iannuccelli, Cristina;Guzzo, Maria Paola;Conti, Fabrizio;Di Franco, Manuela
2019

Abstract

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.
2019
ACPAs; lung; microbiota; mucosal immunity; periodontitis; rheumatoid arthritis
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
Mucosa-Environment Interactions in the Pathogenesis of Rheumatoid Arthritis / Lucchino, Bruno; Spinelli, Francesca Romani; Iannuccelli, Cristina; Guzzo, Maria Paola; Conti, Fabrizio; Di Franco, Manuela. - In: CELLS. - ISSN 2073-4409. - 8:7(2019), p. 700. [10.3390/cells8070700]
File allegati a questo prodotto
File Dimensione Formato  
Lucchino_Mucosa–Environment_2019.pdf

accesso aperto

Tipologia: Versione editoriale (versione pubblicata con il layout dell'editore)
Licenza: Creative commons
Dimensione 773.59 kB
Formato Adobe PDF
773.59 kB Adobe PDF

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1315153
Citazioni
  • ???jsp.display-item.citation.pmc??? 16
  • Scopus 35
  • ???jsp.display-item.citation.isi??? 35
social impact