Serum proinflammatory cytokines directing T helper 1 polarization in patients with familial Mediterranean fever.
Th1 type polarization has been implicated in the pathogenesis of familial Mediterranean fever (FMF). Interleukin-12 (IL-12) and IL-10 are proinflammatory cytokines, which play crucial role in Th1 and Th2 type immune response, respectively. IL-18 has a dual effect on T cell response: it was recognized as an IFN-gamma-inducing factor in T cells; acting in synergy with IL-12, leading to the development of Th1 type immune responses. But, in the absence of IL-12, IL-18 can promote the production of Th2 cytokines and take part in allergic inflammation. The aim of this study is to measure serum levels of IL-10, IL-12, and IL-18 in patients with FMF, and to investigate the relationship of their expressions with FMF attacks. Serum IL-10, IL-12, and IL-18 levels from patients with FMF were investigated. Thirty-one FMF patients with attack-free, 24 FMF patients with attack and 20 healthy controls were enrolled in the study. The levels of IL-10, IL-12p70 and IL-18 were measured by ELISA. Serum IL-10 levels were not different in FMF patients with attack and attack-free, and healthy controls. Serum IL-12 levels in FMF patients both with attack and attack-free were significantly higher than healthy controls (P = 0.002 and P = 0.047, respectively). There were no differences between FMF patients with attack and attack-free with regard to serum IL-12 levels. Serum IL-18 levels in FMF patients with attack and attack-free were significantly higher than healthy controls (P < 0.001 for both groups). With respect to serum IL-18 levels, no difference was found between FMF patients with attack and attack-free. Our results suggest that IL-12 and IL-18 contribute to the establishment of Th1 polarization seen in FMF and play a part in its pathogenesis. Detection of increased levels of IL-12 and IL-18 in patients with inactive disease implies that they seem to assist Th1 activation and subclinical inflammation persisting during the attack-free period of the disease.
Simsek
Ismail
I
Division of Rheumatology, Gulhane Military School of Medicine, Ankara, Turkey. isimsek@gara.edu.tr
Pay
Salih
S
Pekel
Aysel
A
Dinc
Ayhan
A
Musabak
Ugur
U
Erdem
Hakan
H
Sengul
Ali
A
D000328:Adult; D016764:Cell Polarity / Q000276:immunology*; D016207:Cytokines / Q000032:analysis / Q000097:blood / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D010505:Familial Mediterranean Fever / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000276:immunology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood / Q000276:immunology; D016753:Interleukin-10 / Q000032:analysis / Q000097:blood / Q000276:immunology; D018664:Interleukin-12 / Q000032:analysis / Q000097:blood / Q000276:immunology*; D020382:Interleukin-18 / Q000032:analysis / Q000097:blood / Q000276:immunology*; D008297:Male; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D015854:Up-Regulation / Q000276:immunology
D016207:Cytokines; D018836:Inflammation Mediators; D020382:Interleukin-18; D016753:Interleukin-10; D018664:Interleukin-12