作者: Mythily Srinivasan , Don-Jon Summerlin
DOI: 10.1016/J.CLIM.2009.09.001
关键词:
摘要: Inflammatory bowel diseases (IBD) result from dysregulated immune responses to the luminal antigens initiated by colonic epithelial cells (CEC) and propagated activated CD4+ T cells. Biological therapies are being developed that suppress inflammation promote homeostasis. Treatment with CD80-competitive antagonist peptide (CD80-CAP) has been shown cell in multiple disease models. Here we investigated effect of CD80-CAP on CEC experimental colitis. Balb/c mice induced trinitrobenzene sulfonic acid (TNBS) colitis were administered CD80-CAP/control peptide/vehicle. Administration decreased microscopic restored expression TLR-2, 3, 4 5 mRNA physiological levels. Furthermore, treatment suppressed Th1cytokines enhanced Th2 mice. In conclusion, administration ameliorated TNBS reducing inflammatory infiltration modulating response potentially restoring mucosal tolerance.