Abstract
Neutrophils - a complex story in the pathogenesis of systemic lupus erythematosus
Highlights
Prevention of systemic lupus erythematosus (SLE) presents many challenges
In further studies we have demonstrated that the BANK1 splice variant is associated with significantly reduced expression of the Δ2 isoform and that the risk haplotype is further associated with blunted proximal BCR signaling in naïve B cells and enhanced p-AKT in memory B cells
In multivariable regression analyses controlling for age and years since diagnosis, we found a significant interaction between unfair treatment and attributions to racial discrimination (b = -0.52, SE = 0.24, P = 0.03)
Summary
Prevention of systemic lupus erythematosus (SLE) presents many challenges. By contrast, prevention of acquired immunodeficiency syndrome (AIDS) is relatively straightforward: an infective agent has been identified, risk behaviors are well-delineated, antiviral therapeutics are highly effective and neonates have been apparently cured. We are interested in understanding the role of IRF5 in human B cells since previous studies in mice implicated a role for IRF5 in effector B-cell development and function and murine models of lupus lacking the Irf gene showed reduced ANA, glomerulonephritis and pathogenic autoantibody production. Conclusions: These results identify mTOR activation to be a trigger of IL-4 production and necrotic death of DN T cells, predictor of disease flares, and effective target for treatment in patients with SLE. Methods: TLR7-mediated experimental lupus was induced in wild-type and knockout mice by pristane and the expression of IFN-I stimulated genes and numbers of plasmacytoid dendritic cells (pDCs) and inflammatory (Ly6Chi) monocytes were assessed by PCR and flow cytometry, respectively. BILAG and SELENA SLEDAI flares and corticosteroid usage were assessed 4 weekly
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