| First Author | Su H | Year | 2005 |
| Journal | Science | Volume | 307 |
| Issue | 5714 | Pages | 1465-8 |
| PubMed ID | 15746428 | Mgi Jnum | J:96645 |
| Mgi Id | MGI:3531073 | Doi | 10.1126/science.1104765 |
| Citation | Su H, et al. (2005) Requirement for caspase-8 in NF-kappaB activation by antigen receptor. Science 307(5714):1465-8 |
| abstractText | Caspase-8, a proapoptotic protease, has an essential role in lymphocyte activation and protective immunity. We show that caspase-8 deficiency (CED) in humans and mice specifically abolishes activation of the transcription factor nuclear factor kappaB (NF-kappaB) after stimulation through antigen receptors, Fc receptors, or Toll-like receptor 4 in T, B, and natural killer cells. Caspase-8 also causes the alphabeta complex of the inhibitor of NF-kappaB kinase (IKK) to associate with the upstream Bcl10-MALT1 (mucosa-associated lymphatic tissue) adapter complex. Recruitment of the IKKalpha, beta complex, its activation, and the nuclear translocation of NF-kappaB require enzyme activity of full-length caspase-8. These findings thus explain the paradoxical association of defective apoptosis and combined immunodeficiency in human CED. |
