Open AccessAnalysis of serum interleukin( IL )‐1α, IL ‐1β and IL ‐18 in patients with systemic sclerosis
Author(s) -
Lin Emily,
Vincent Fabien B,
Sahhar Joanne,
Ngian GeneSiew,
KandaneRathnayake Rangi,
Mende Rachel,
Morand Eric F,
Lang Tali,
Harris James
Publication year - 2019
Publication title -
clinical and translational immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.321
H-Index - 34
ISSN - 2050-0068
DOI - 10.1002/cti2.1045
Subject(s) - immunology , interleukin 15 , interleukin , medicine , cytokine
Objectives Systemic sclerosis ( SS c) is an autoimmune disease characterised by fibrosis, vascular dysfunction and immune dysregulation. The pathogenesis of SS c remains poorly understood, although studies have indicated a role for the innate immune response. Methods Here, we measured serum interleukin ( IL )‐1α, IL ‐1β and IL ‐18 levels in 105 SS c patients and 47 healthy controls ( HC ) and analysed them with respect to multiple clinical parameters. Results Serum IL ‐18 concentrations were significantly higher in SS c patients than in HC , while no significant differences in concentrations of IL ‐1α and IL ‐1β were observed between SS c and HC . In both SS c and HC serum, IL ‐1α and IL ‐1β were positively correlated, while in SS c, both cytokines negatively correlated with IL ‐18. Serum IL ‐18 was significantly negatively correlated with both carbon monoxide transfer coefficient ( KCO ) and diffusing capacity of the lungs for carbon monoxide ( DLCO ). Serum IL ‐1β was positively correlated with the modified Rodnan skin score ( mRSS ), particularly in patients with limited subtype. DLCO , KCO and tricuspid regurgitation ( TR ) velocity were significantly higher in patients with high serum IL ‐1β. Serum IL ‐1α was significantly lower in SS c patients with low KCO and positively correlated with KCO . SS c patients with high serum IL ‐1α concentrations were more likely to have digital ulcers. Conclusions Our data suggest that these IL ‐1 family cytokines may have different roles in the pathogenesis of SS c fibrotic complications.