NOD2 regulates hematopoietic cell function during graft-versus-host disease Academic Article uri icon


MeSH Major

  • Graft vs Host Disease
  • Hematopoietic System
  • Nod2 Signaling Adaptor Protein


  • Nucleotide-binding oligomerization domain 2 (NOD2) polymorphisms are independent risk factors for Crohn's disease and graft-versus-host disease (GVHD). In Crohn's disease, the proinflammatory state resulting from NOD2 mutations have been associated with a loss of antibacterial function of enterocytes such as paneth cells. NOD2 has not been studied in experimental allogeneic bone marrow transplantation (allo-BMT). Using chimeric recipients with NOD2(-/-) hematopoietic cells, we demonstrate that NOD2 deficiency in host hematopoietic cells exacerbates GVHD. We found that proliferation and activation of donor T cells was enhanced in NOD-deficient allo-BMT recipients, suggesting that NOD2 plays a role in the regulation of host antigen-presenting cells (APCs). Next, we used bone marrow chimeras in an experimental colitis model and observed again that NOD2 deficiency in the hematopoietic cells results in increased intestinal inflammation. We conclude that NOD2 regulates the development of GVHD through its inhibitory effect on host APC function.

publication date

  • September 28, 2009



  • Academic Article



  • eng

PubMed Central ID

  • PMC2757869

Digital Object Identifier (DOI)

  • 10.1084/jem.20090623

PubMed ID

  • 19737867

Additional Document Info

start page

  • 2101

end page

  • 10


  • 206


  • 10