Inflammatory bowel disease requires the interplay between innate and adaptive immune signals

Dayna Shi, Jyoti Das, Gobardhan Das

Research output: Contribution to journalArticle

35 Scopus citations

Abstract

Inflammatory bowl disease (IBD) is a type 1 T helper cell (Th1)-mediated autoimmune disease. Various studies have revealed that environmental pathogens also play a significant role in the initiation and progression of this disease. Interestingly, the pathogenesis of IBD has been shown to be related to nitric oxide (NO) released from innate immune cells. Although NO is known to be highly toxic to the gut epithelia, there is very little information about the regulation of NO production, One major question in the etiology of IBD is how Th1 cells and pathogens interact in the induction of IBD. In present study, we focused on the regulation of NO. We show that macrophages require both interferon-γ (IFN-γ)-mediated and TLR4-mediated signals for the production of NO, which causes inflammation in the intestine and subsequently IBD. Thus, IBD is the result of concerted actions of innate immune signals, such as the binding of LPS to TLR-4, and adaptive immune signals, such as IFN-γ produced by Th1 cells.

Original languageEnglish (US)
Pages (from-to)70-74
Number of pages5
JournalCell Research
Volume16
Issue number1
DOIs
StatePublished - Jan 19 2006

Keywords

  • Adaptive immunity
  • Colitis
  • Innate immunity
  • Nitric oxide
  • TLR-mediated signaling

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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