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Aim: Depletion of TLR4 in β-cells leads to long-term survival in a mouse allogeneneic β-cells transplantation model.The aim of this study is to develop an applicable approach to block TLR4 activation in β-cells using a blocking peptide for TLR4 to improve the survival and function of β-cells in vitro and in vivo.Materials and Methods: A 33 amino acids peptide that contains the protein transfer domain of Hph-1 virus (YARVRRRGPRR) together with the amino acids identical to the 702 to 723 of TLR4 protein in the C3H/HeJ mice were generated and named Hph-1-dnTLR4 blocking peptide.The insulinoma cell line, βTC3 cells were pre-incubated with the Hph-1-dnTLR4 or an irrelevant control peptides at 100nM for 1-24 hr and stimulated with ultra pure LPS (100ng/ml, Invivogen, San Diego, CA) or proinflammatory cytokines (IL-1b and INF-r).