The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis

Differences in clinical presentation, response to treatment, and long-term outcomes between autoantibody-positive and -negative rheumatoid arthritis (RA) highlight the need for a better comprehension of the immunopathogenic events underlying the two disease subtypes. Whilst the drivers and perpetuat...

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Autores principales:	Ludovico De Stefano, Bernardo D’Onofrio, Antonio Manzo, Carlomaurizio Montecucco, Serena Bugatti
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	rheumatoid arthritis seronegative anti-citrullinated protein antibodies rheumatoid factor pathogenesis Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/0cea7045e9544de1be5ab9bbd3737fb5
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spelling	oai:doaj.org-article:0cea7045e9544de1be5ab9bbd3737fb52021-11-25T17:56:08ZThe Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis10.3390/ijms2222123861422-00671661-6596https://doaj.org/article/0cea7045e9544de1be5ab9bbd3737fb52021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12386https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Differences in clinical presentation, response to treatment, and long-term outcomes between autoantibody-positive and -negative rheumatoid arthritis (RA) highlight the need for a better comprehension of the immunopathogenic events underlying the two disease subtypes. Whilst the drivers and perpetuators of autoimmunity in autoantibody-positive RA have started to be disclosed, autoantibody-negative RA remains puzzling, also due its wide phenotypic heterogeneity and its possible misdiagnosis. Genetic susceptibility appears to mostly rely on class I HLA genes and a number of yet unidentified non-HLA loci. On the background of such variable genetic predisposition, multiple exogeneous, endogenous, and stochastic factors, some of which are not shared with autoantibody-positive RA, contribute to the onset of the inflammatory cascade. In a proportion of the patients, the immunopathology of synovitis, at least in the initial stages, appears largely myeloid driven, with abundant production of proinflammatory cytokines and only minor involvement of cells of the adaptive immune system. Better understanding of the complexity of autoantibody-negative RA is still needed in order to open new avenues for targeted intervention and improve clinical outcomes.Ludovico De StefanoBernardo D’OnofrioAntonio ManzoCarlomaurizio MontecuccoSerena BugattiMDPI AGarticlerheumatoid arthritisseronegativeanti-citrullinated protein antibodiesrheumatoid factorpathogenesisBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12386, p 12386 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	rheumatoid arthritis seronegative anti-citrullinated protein antibodies rheumatoid factor pathogenesis Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	rheumatoid arthritis seronegative anti-citrullinated protein antibodies rheumatoid factor pathogenesis Biology (General) QH301-705.5 Chemistry QD1-999 Ludovico De Stefano Bernardo D’Onofrio Antonio Manzo Carlomaurizio Montecucco Serena Bugatti The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis
description	Differences in clinical presentation, response to treatment, and long-term outcomes between autoantibody-positive and -negative rheumatoid arthritis (RA) highlight the need for a better comprehension of the immunopathogenic events underlying the two disease subtypes. Whilst the drivers and perpetuators of autoimmunity in autoantibody-positive RA have started to be disclosed, autoantibody-negative RA remains puzzling, also due its wide phenotypic heterogeneity and its possible misdiagnosis. Genetic susceptibility appears to mostly rely on class I HLA genes and a number of yet unidentified non-HLA loci. On the background of such variable genetic predisposition, multiple exogeneous, endogenous, and stochastic factors, some of which are not shared with autoantibody-positive RA, contribute to the onset of the inflammatory cascade. In a proportion of the patients, the immunopathology of synovitis, at least in the initial stages, appears largely myeloid driven, with abundant production of proinflammatory cytokines and only minor involvement of cells of the adaptive immune system. Better understanding of the complexity of autoantibody-negative RA is still needed in order to open new avenues for targeted intervention and improve clinical outcomes.
format	article
author	Ludovico De Stefano Bernardo D’Onofrio Antonio Manzo Carlomaurizio Montecucco Serena Bugatti
author_facet	Ludovico De Stefano Bernardo D’Onofrio Antonio Manzo Carlomaurizio Montecucco Serena Bugatti
author_sort	Ludovico De Stefano
title	The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis
title_short	The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis
title_full	The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis
title_fullStr	The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis
title_full_unstemmed	The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis
title_sort	genetic, environmental, and immunopathological complexity of autoantibody-negative rheumatoid arthritis
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/0cea7045e9544de1be5ab9bbd3737fb5
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The Genetic, Environmental, and Immunopathological Complexity of Autoantibody-Negative Rheumatoid Arthritis

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