Modulation of the colonic epithelial cell responses and amelioration of inflammation by CD80 blockade in TNBS colitis

Mythily Srinivasan, Don Jon Summerlin

Research output: Contribution to journalArticle

9 Scopus citations


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 Th1cytokines 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.

Original languageEnglish (US)
Pages (from-to)411-421
Number of pages11
JournalClinical Immunology
Issue number3
StatePublished - Dec 1 2009



  • Apoptosis
  • CD80 blockade
  • Colitis
  • Intestinal epithelial cells
  • Toll-like receptors

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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