Abstract |
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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Authors | Giuseppe Lopalco, Luca Cantarini, Antonio Vitale, Florenzo Iannone, Maria Grazia Anelli, Laura Andreozzi, Giovanni Lapadula, Mauro Galeazzi, Donato Rigante |
Journal | Mediators of inflammation
(Mediators Inflamm)
Vol. 2015
Pg. 194864
( 2015)
ISSN: 1466-1861 [Electronic] United States |
PMID | 25784780
(Publication Type: Journal Article, Review)
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Chemical References |
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Topics |
- Adaptive Immunity
(physiology)
- Animals
- Autoimmune Diseases
(metabolism)
- Autoimmunity
(physiology)
- Hereditary Autoinflammatory Diseases
(metabolism)
- Humans
- Interleukin-1
(metabolism)
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