Interleukin-1 as a common denominator from autoinflammatory to autoimmune disorders: premises, perils, and perspectives

Mediators of Inflammation
Giuseppe LopalcoDonato Rigante

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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Methods Mentioned

BETA
exome sequencing
bronchoalveolar lavage

Clinical Trials Mentioned

NCT01327846
NCT01144975
NCT01066715
NCT00513214
NCT01684345
NCT01747538
NCT01965145
NCT01835132
NCT02219828
NCT01441076

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