Increased peripheral proinflammatory T helper subsets contribute to cardiovascular complications in diabetic patients.

Background: Coronary atherosclerotic heart disease (CHD) is one of the major concerns in type 2 diabetes (T2D). The systemic chronic inflammation has been postulated to bridge the increased risk of cardiovascular disease and T2D. We formulated that increased peripheral proinflammatory T helper subsets contributed to the development of cardiovascular complications in diabetic patients.

[Effects of Foxp3 knockdown on the functions of human regulatory T cells].

Objective: To employ the technology of interfering RNA (RNAi) to identify the role of Foxp3 in the in vitro suppressive effect of human regulatory T cell (Treg) on effector T cells.

Methods: Expanded human Treg were transfected with siRNA targeting Foxp3 genes. The transfection efficiency, the level of corresponding gene and its protein expression were measured by fluorescent microscopy, fluorescence-activated cell sorting (FACS), real-time PCR and Western blot respectively.

Association between islet xenograft rejection mediated by activated macrophages and upregulated chemokines.

Objective: Our previous study has shown that porcine antigen-primed and CD4+ T cells activated macrophages are capable of the Recognition and rejection of porcine xenografts but not mouse allografts, and therefore suggested the involvement of signaling between the graft and macrophages in this specific graft recognition and destruction.

Methods: NOD-SCID mice were transplanted with fetal pig pancreatic fragment (FPP) before adoptive transfer with exogenous macrophages isolated from rejecting FPP xenografts of BALB/c recipient mice. The exogenous macrophages were tracked by Ly5.