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Rheumatology Image Library:This section of synovial membrane from a patient with systemic lupus erythematosus shows mild chronic synovitis. There is hyperplasia of synovial lining cells. Via Krishan Maggon 
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Pfizer Inc. announced today that it will present data for several of its marketed and investigational medicines for inflammatory and immunological conditions at the American College of Rheumatology (ACR) / Association of Rheumatology Health Professionals (ARHP) 2014 Annual Meeting (November 14-19, Boston, Massachusetts). Via Krishan Maggon
Krishan Maggon 's curator insight,
November 13, 2014 3:11 AM
Improvement of disease activity and reduction of severe flares following subcutaneous administration of an IL-6 monoclonal antibody (mAb) in subjects with active generalized systemic lupus erythematosus (SLE)." Wallace DJ, Popa S, Spindler AJ, et. al. [Presentation L3; November 18, 2014 5:00 p.m. - 5:15 p.m.] Add to the Body of Evidence for XELJANZ® (Tofacitinib Citrate) as a Treatment Option for Adults with Moderate to Severe Rheumatoid Arthritis- - - Efficacy Results from a Phase 2 Study of Anti-IL-6 in Patients with Systemic Lupus Erythematosus- - - Phase 1 Abstracts for Two Pfizer Biosimilars in Development; Both Assets Move into Phase 3 Comparability Trials |
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Elevated concentrations of inflammatory mediators are characteristic of autoimmune disease accompanied by chronic or recurrent inflammation. We examined the hypothesis that mediators of inflammation known to be elevated in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are associated with genetic polymorphism previously identified in studies of inflammatory disease. Serum interleukin 6 (IL-6) and tumor necrosis factor alpha (TNFα) concentrations in patients with SLE (n = 117) or RA (n = 164) and in inflammatory disease-free control subjects (n = 172) were measured by multiplex ELISA. Candidate genes were chosen from studies of autoimmune and inflammatory disease. Genotypes were determined for 345 SNP markers in 75 genes. Association between serum analytes and single alleles was tested by linear regression. Polymorphisms in several genes were associated with IL-6 levels (including IL10, TYK2, and CD40L in SLE and DRB1, NOD2, and CSF1 in RA) or with TNFα levels (including TNFSF4 and CSF2 in SLE and PTPN2, DRB1, and NOD2 in RA). Some associations were shared between disease and control groups or between IL-6 and TNFα within a group.
In conclusion, variation in genes implicated in disease pathology is associated with serum IL-6 or TNFα concentration. Some genetic associations are more apparent in healthy controls than in SLE or RA, suggesting dysregulation of the principal mediators of chronic inflammation in disease. Susceptibility genes may affect inflammatory response with variable effect on disease etiology. Via Edward NS, Krishan Maggon
Edward NS's curator insight,
February 16, 2015 11:55 AM
Clinical Rheumatology February 2015Solus JF1, Chung CP, Oeser A, Li C, Rho YH, Bradley KM, Kawai VK, Smith JR, Stein CM.Division of Rheumatology, Vanderbilt University, Nashville, TN, USA
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