| First Author | Dejardin E | Year | 2002 |
| Journal | Immunity | Volume | 17 |
| Issue | 4 | Pages | 525-35 |
| PubMed ID | 12387745 | Mgi Jnum | J:79573 |
| Mgi Id | MGI:2388509 | Doi | 10.1016/s1074-7613(02)00423-5 |
| Citation | Dejardin E, et al. (2002) The Lymphotoxin-beta Receptor Induces Different Patterns of Gene Expression via Two NF-kappaB Pathways. Immunity 17(4):525 |
| abstractText | The lymphotoxin-beta receptor (LTbetaR) plays critical roles in inflammation and lymphoid organogenesis through activation of NF-kappaB. In addition to activation of the classical NF-kappaB, ligation of this receptor induces the processing of the cytosolic NF-kappaB2/p100 precursor to yield the mature p52 subunit, followed by translocation of p52 to the nucleus. This activation of NF-kappaB2 requires NIK and IKKalpha, while NEMO/IKKgamma is dispensable for p100 processing. IKKbeta-dependent activation of canonical NF-kappaB is required for the expression but not processing of p100 and for the expression of proinflammatory molecules including VCAM-1, MIP-1beta, and MIP-2 in response to LTbetaR ligation. In contrast, IKKalpha controls the induction by LTbetaR ligation of chemokines and cytokines involved in lymphoid organogenesis, including SLC, BLC, ELC, SDF1, and BAFF. |
