Interleukin-1 as a Common Denominator from Autoinflammatory to Autoimmune Disorders: Premises, Perils, and Perspectives

A complex web of dynamic relationships between innate and adaptive immunity is now evident for many autoinflammatory and autoimmune disorders, the first deriving from abnormal activation of innate immune system without any conventional danger triggers and the latter from self-/non-self-discriminatio...

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Main Authors: Giuseppe Lopalco, Luca Cantarini, Antonio Vitale, Florenzo Iannone, Maria Grazia Anelli, Laura Andreozzi, Giovanni Lapadula, Mauro Galeazzi, Donato Rigante
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2015/194864
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author Giuseppe Lopalco
Luca Cantarini
Antonio Vitale
Florenzo Iannone
Maria Grazia Anelli
Laura Andreozzi
Giovanni Lapadula
Mauro Galeazzi
Donato Rigante
author_facet Giuseppe Lopalco
Luca Cantarini
Antonio Vitale
Florenzo Iannone
Maria Grazia Anelli
Laura Andreozzi
Giovanni Lapadula
Mauro Galeazzi
Donato Rigante
author_sort Giuseppe Lopalco
collection DOAJ
description A complex web of dynamic relationships between innate and adaptive immunity is now evident for many autoinflammatory and autoimmune disorders, the first deriving from abnormal activation of innate immune system without any conventional danger triggers and the latter from self-/non-self-discrimination loss of tolerance, and systemic inflammation. Due to clinical and pathophysiologic similarities giving a crucial role to the multifunctional cytokine interleukin-1, the concept of autoinflammation has been expanded to include nonhereditary collagen-like diseases, idiopathic inflammatory diseases, and metabolic diseases. As more patients are reported to have clinical features of autoinflammation and autoimmunity, the boundary between these two pathologic ends is becoming blurred. An overview of monogenic autoinflammatory disorders, PFAPA syndrome, rheumatoid arthritis, type 2 diabetes mellitus, uveitis, pericarditis, Behçet’s disease, gout, Sjögren’s syndrome, interstitial lung diseases, and Still’s disease is presented to highlight the fundamental points that interleukin-1 displays in the cryptic interplay between innate and adaptive immune systems.
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institution Kabale University
issn 0962-9351
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publishDate 2015-01-01
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series Mediators of Inflammation
spelling doaj-art-03213e9266f740e8a0d8cc39c32c08872025-02-03T01:25:28ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/194864194864Interleukin-1 as a Common Denominator from Autoinflammatory to Autoimmune Disorders: Premises, Perils, and PerspectivesGiuseppe Lopalco0Luca Cantarini1Antonio Vitale2Florenzo Iannone3Maria Grazia Anelli4Laura Andreozzi5Giovanni Lapadula6Mauro Galeazzi7Donato Rigante8Interdisciplinary Department of Medicine, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, ItalyResearch Center of Systemic Autoimmune and Autoinflammatory Diseases, University of Siena, Viale Bracci 1, 53100 Siena, ItalyResearch Center of Systemic Autoimmune and Autoinflammatory Diseases, University of Siena, Viale Bracci 1, 53100 Siena, ItalyInterdisciplinary Department of Medicine, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, ItalyInterdisciplinary Department of Medicine, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, ItalyInstitute of Pediatrics, Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168 Rome, ItalyInterdisciplinary Department of Medicine, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, ItalyResearch Center of Systemic Autoimmune and Autoinflammatory Diseases, University of Siena, Viale Bracci 1, 53100 Siena, ItalyInstitute of Pediatrics, Università Cattolica del Sacro Cuore, Largo Agostino Gemelli 8, 00168 Rome, ItalyA complex web of dynamic relationships between innate and adaptive immunity is now evident for many autoinflammatory and autoimmune disorders, the first deriving from abnormal activation of innate immune system without any conventional danger triggers and the latter from self-/non-self-discrimination loss of tolerance, and systemic inflammation. Due to clinical and pathophysiologic similarities giving a crucial role to the multifunctional cytokine interleukin-1, the concept of autoinflammation has been expanded to include nonhereditary collagen-like diseases, idiopathic inflammatory diseases, and metabolic diseases. As more patients are reported to have clinical features of autoinflammation and autoimmunity, the boundary between these two pathologic ends is becoming blurred. An overview of monogenic autoinflammatory disorders, PFAPA syndrome, rheumatoid arthritis, type 2 diabetes mellitus, uveitis, pericarditis, Behçet’s disease, gout, Sjögren’s syndrome, interstitial lung diseases, and Still’s disease is presented to highlight the fundamental points that interleukin-1 displays in the cryptic interplay between innate and adaptive immune systems.http://dx.doi.org/10.1155/2015/194864
spellingShingle Giuseppe Lopalco
Luca Cantarini
Antonio Vitale
Florenzo Iannone
Maria Grazia Anelli
Laura Andreozzi
Giovanni Lapadula
Mauro Galeazzi
Donato Rigante
Interleukin-1 as a Common Denominator from Autoinflammatory to Autoimmune Disorders: Premises, Perils, and Perspectives
Mediators of Inflammation
title Interleukin-1 as a Common Denominator from Autoinflammatory to Autoimmune Disorders: Premises, Perils, and Perspectives
title_full Interleukin-1 as a Common Denominator from Autoinflammatory to Autoimmune Disorders: Premises, Perils, and Perspectives
title_fullStr Interleukin-1 as a Common Denominator from Autoinflammatory to Autoimmune Disorders: Premises, Perils, and Perspectives
title_full_unstemmed Interleukin-1 as a Common Denominator from Autoinflammatory to Autoimmune Disorders: Premises, Perils, and Perspectives
title_short Interleukin-1 as a Common Denominator from Autoinflammatory to Autoimmune Disorders: Premises, Perils, and Perspectives
title_sort interleukin 1 as a common denominator from autoinflammatory to autoimmune disorders premises perils and perspectives
url http://dx.doi.org/10.1155/2015/194864
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