Journal article
Interleukin-6 trans-signaling exacerbates inflammation and renal pathology in lupus-prone mice
E Tsantikos, MJ Maxwell, T Putoczki, M Ernst, S Rose-John, DM Tarlinton, ML Hibbs
Arthritis and Rheumatism | Published : 2013
DOI: 10.1002/art.38061
Abstract
Objective Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease that is characterized by the production of antinuclear antibodies (ANAs) and leads to immune complex deposition in the kidneys and nephritis. Lyn tyrosine kinase is a regulator of antibody-mediated autoimmune disease, as evidenced by studies in gene-targeted mice and as suggested in genome-wide association studies in SLE. Like SLE patients, Lyn-deficient mice have increased levels of interleukin-6 (IL-6). Deletion of IL-6 from Lyn-deficient mice abrogates levels of inflammation, pathogenic autoantibodies, and nephritis. The purpose of this study was to assess the role of IL-6 trans-signaling in autoimmune dise..
View full abstractGrants
Awarded by DFG
Funding Acknowledgements
Supported by grants from the National Health and Medical Research Council of Australia (NHMRC), by Operational Infrastructure Support from the state government of Victoria, and by the Independent Research Institutes Infrastructure Support Scheme from the NHMRC. Drs. Maxwell, Ernst, Tarlinton, and Hibbs are Research Fellows of the NHMRC. Dr. Rose-John's work was supported by the DFG (SFB877, project A1) and by the Cluster of Excellence program (Inflammation at Interfaces project).