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Nod2 deficiency is associated with an increased mucosal immunoregulatory response to commensal microorganisms.

Abstract
On the basis of previous studies demonstrating that a breach of the colonic epithelial barrier is associated with a microbiota-dependent increase in lamina propria (LP) regulatory cells, we investigated if the lack of spontaneous intestinal inflammation observed in nucleotide-binding oligomerization domain 2 (Nod2)-/- mice was due to enhanced intestinal regulatory function. We found that the LP CD4+ T-cell population of Nod2-/- mice contains an increased percentage of CD4+ regulatory T cells bearing transforming growth factor -β/latency peptide (LP CD4+LAP (latency-associated peptide) + T cells) both under baseline conditions and following an intentional breach of the colonic barrier induced by ethanol administration. In addition, we found that Nod2-/- mice manifest decreased severity of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-colitis and that TNBS-colitis in Nod2-/- or Nod2+/+ mice is ameliorated by adoptive transfer of LP cells from ethanol-treated mice before, but not after, depletion of LAP+ T cells. This increased regulatory T-cell response in Nod2-/- mice could explain why NOD2 polymorphisms in humans are not in themselves sufficient to establish inflammatory lesions.
AuthorsA Amendola, A Butera, M Sanchez, W Strober, M Boirivant
JournalMucosal immunology (Mucosal Immunol) Vol. 7 Issue 2 Pg. 391-404 (Mar 2014) ISSN: 1935-3456 [Electronic] United States
PMID23962873 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • CD11c Antigen
  • Nod2 Signaling Adaptor Protein
Topics
  • Adoptive Transfer
  • Animals
  • CD11c Antigen (metabolism)
  • Colitis (chemically induced, immunology, metabolism, microbiology)
  • Colon (immunology, metabolism, pathology)
  • Dendritic Cells (immunology, metabolism)
  • Immunomodulation (genetics)
  • Intestinal Mucosa (immunology, metabolism, microbiology)
  • Male
  • Mice
  • Mice, Knockout
  • Microbiota
  • Nod2 Signaling Adaptor Protein (deficiency)
  • Permeability
  • T-Lymphocyte Subsets (immunology, metabolism)

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