Our news editors obtained a quote from the research from Haukeland Hospital, "CXCL10 is also elevated in the serum of Addison's disease patients. We therefore investigated if the viral RNA substitute polyinosine-polycytidylic acid (poly (I:C)) could influence the cytokine induced production of CXCL10 by adrenocortical cells. We found that poly (I:C) could induce CXCL10 in NCI-H295R adrenocortical carcinoma cells, either alone or synergistically along with cytokines interferon-gamma and tumor necrosis factor-alpha. This effect was found to be mediated by toll-like receptor 3 and both nuclear factor kappa B (NF kappa B) and signal transducer and activator of transcription-1 (STAT1), but not type I interferons, seemed to be involved."
According to the news editors, the research concluded: "We propose that the combination of environmental and endogenous factors presented here, could contribute to the multifactorial pathogenesis of autoimmune Addison's disease."
For more information on this research see: Induction of CXCL10 chemokine in adrenocortical cells by stimulation through toll-like receptor 3. Molecular and Cellular Endocrinology, 2013;365(1):75-83. Molecular and Cellular Endocrinology can be contacted at: Elsevier Ireland Ltd, Elsevier House, Brookvale Plaza, East Park Shannon, Co, Clare, 00000, Ireland. (Elsevier - www.elsevier.com; Molecular and Cellular Endocrinology - www.elsevier.com/wps/product/cws_home/506028)
The news editors report that additional information may be obtained by contacting E. Bratland, Haukeland Hosp, Dept. of Med, N-5021 Bergen, Norway.
Keywords for this news article include: Bergen, Norway, Europe, Peptides, Immunology, Endocrinology, CXC Chemokines, Addison Disease, Chemokine CXCL10, Membrane Proteins, Biological Factors, Cytokine Receptors, Chemokine Receptors, Chemotactic Factors, Toll-Like Receptor 3, Adrenal Insufficiency, Adrenal Gland Diseases, Inflammation Mediators
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