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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)α 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 …
Competing interests: None.
Funding: This research was funded by The Health and Medical Care Executive Board of the Västra Götaland, Rune och Ulla Amlövs foundation for Rheumatology Research, Göteborg’s Association Against Rheumatism, Reumaforskningsfond Margareta, The Medical Society of Göteborg, the Medical Faculty of Göteborg (LUA) and Finska Läkaresällskapet, HUS TYH 2235 evo grant, Invalid Foundation, the Finnish Dental Society Apollonia, CIMO and Helsinki University.
Ethics approval: Patients gave informed written consent and the study was approved by the local Ethics Committee.
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