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• W1994152080 abstract "Inflammatory bowel diseases (IBD) result from dysregulated immune responses to the luminal antigens initiated by the colonic epithelial cells (CEC) and propagated by activated CD4+ T cells. Biological therapies are being developed that suppress inflammation and promote epithelial homeostasis. Treatment with the CD80-competitive antagonist peptide (CD80-CAP) has been shown to suppress T cell responses in multiple disease models. Here we investigated the effect of the CD80-CAP on the CEC responses in experimental colitis. Balb/c mice induced with trinitrobenzene sulfonic acid (TNBS) colitis were administered CD80-CAP/control peptide/vehicle. Administration of the CD80-CAP decreased microscopic inflammation and restored the expression of TLR-2, 3, 4 and 5 mRNA in the CEC of colitis mice to physiological levels. Furthermore, the CD80-CAP treatment suppressed Th1 cytokines and enhanced Th2 responses by the CEC in colitis mice. In conclusion, CD80-CAP administration ameliorated TNBS colitis by reducing the inflammatory cell infiltration and modulating the CEC response potentially restoring mucosal tolerance." @default.
• W1994152080 created "2016-06-24" @default.
• W1994152080 creator A5016850831 @default.
• W1994152080 creator A5069148100 @default.
• W1994152080 date "2009-12-01" @default.
• W1994152080 modified "2023-09-26" @default.
• W1994152080 title "Modulation of the colonic epithelial cell responses and amelioration of inflammation by CD80 blockade in TNBS colitis" @default.
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• W1994152080 doi "https://doi.org/10.1016/j.clim.2009.09.001" @default.
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