B cells promote inflammation in obesity and type 2 diabetes through regulation of T-cell function and an inflammatory cytokine profile

摘要: Patients with type 2 diabetes (T2D) have disease-associated changes in B-cell function, but the role these play disease pathogenesis is not well established. Data herein show B cells from obese mice produce a proinflammatory cytokine profile compared lean mice. Complementary vivo studies that cell–null decreased systemic inflammation, inflammatory B- and T-cell cytokines, adipose tissue insulin resistance (IR) WT Reduced inflammation obese/insulin resistant associates an increased percentage of anti-inflammatory regulatory T (Tregs). This increase contrasts sharply Tregs suggests may be critical regulators functions previously shown to important roles IR. We demonstrate T2D (but non-T2D) subjects support function obesity/T2D through contact-dependent mechanisms. In contrast, human monocytes cytokines both non-T2D analyses. These data conclusion are due their direct ability promote secrete profile. Thus, potential therapeutic targets for T2D.