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- Title
Is BID required for NOD signalling?
- Authors
Nachbur, Ueli; Vince, James E.; O'Reilly, Lorraine A.; Strasser, Andreas; Silke, John
- Abstract
Arising from G. Yeretssian et al. 474, 96-99 (2011).Innate immune signalling mediated by the nucleotide-binding and oligomerization domain (NOD) receptors for pathogen-associated constituents regulates the response to intracellular peptidoglycans present in Gram-negative and Gram-positive bacteria. Recently, Yeretssian et al. reported that the pro-apoptotic BH3-only BCL2 family member BID is essential for NOD-mediated immune signalling. This was on the basis of their finding that bone marrow-derived macrophages (BMDMs) from Bid?/? mice failed to activate NF-?B and extracellular signal-regulated kinase (ERK), and were unable to secrete inflammatory cytokines after stimulation with NOD ligands, and that BID-deficient mice were also defective in mounting a cytokine response to in vivo challenge with NOD ligands. Using the same strain of Bid?/? mice used by Yeretssian et al., we found that the mice responded like wild-type mice to NOD ligands, and that the levels of NF-?B or ERK activation and cytokine secretion from Bid?/? BMDMs were indistinguishable from the wild-type response. We therefore propose that the non-apoptotic role of BID in inflammation and innate immunity should be reassessed.
- Subjects
OLIGOMERIZATION; LABORATORY mice; EXTRACELLULAR signal-regulated kinases; GRAM-negative bacteria; PEPTIDOGLYCANS
- Publication
Nature, 2012, Vol 488, Issue 7412, pE4
- ISSN
0028-0836
- Publication type
Article
- DOI
10.1038/nature11366