Interleukin 6 and its soluble receptor in a central role at the neuroimmunoendocrine interface in Sjögren syndrome: an explanatory interventional study

H Forsblad d'Elia¹, C Bjurman^1,2, E Rehnberg^1,3, G Kvist⁴, Y T Konttinen^5,6,7

¹ Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden
² Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden
³ Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden
⁴ Department of Rheumatology, Borås Hospital, Borås, Sweden
⁵ Department of Medicine, Institute of Clinical Medicine, Helsinki University Central Hospital, Helsinki, Finland
⁶ ORTON Orthopedic Hospital of the Invalid Foundation, Helsinki, Finland
⁷ COXA Hospital for Joint Replacement, Tampere, Finland

Correspondence to:
H Forsblad d'Elia, Department of Rheumatology and Inflammation Research, Guldhedsgatan 10A, S-413 46 Göteborg, Sweden; helena.forsblad@vgregion.se

Accepted 24 April 2008

The first 150 words of the full text of this article appear below.

Sjögren syndrome (SS) is characterised by focal adenitis and fatigue, the latter often the most important symptom.¹ Host reactions and responses to disease and disease-associated fatigue consists of stimulation of cytokine network, which involves tumour necrosis factor (TNF) and interleukin (IL)1β, with IL6 often acting as the end stage effector cytokine in this cascade.² Stimulation of host IL6 stimulates protective host responses such as acute phase response and hypothalamus–pituitary–adrenal (HPA) axis. IL6 stimulates hypothalamic corticotropin releasing hormone, pituitary corticotropin and adrenal steroid hormone synthesis.^{3 4} Soluble IL6 receptor (sIL6R) is an agonist to IL6 as IL6 upon binding to sIL6R further binds to signal transducing gp130 protein activating cells that lack membrane bound IL6R. Thus, sIL6R may function as a powerful enhancer of IL6.⁵

The hypothesis of the present study was that IL6 and the HPA axis form a link between the disease and fatigue associated with it, if low serum . . . [Full text of this article]

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