TY - JOUR
T1 - The lymphotoxin-β receptor induces different patterns of gene expression via two NF-κB pathways
AU - Dejardin, Emmanuel
AU - Droin, Nathalie M.
AU - Delhase, Mireille
AU - Haas, Elvira
AU - Cao, Yixue
AU - Makris, Constantin
AU - Li, Zhi Wei
AU - Karin, Michael
AU - Ware, Carl F.
AU - Green, Douglas R.
N1 - Funding Information:
This work was supported by National Institutes of Health Grants CA69381 and AI44828 to D.R.G., NIH CA69381, AI03368, and AI48073 to C.F.W., and NIH ES04151, AI43477, and grant 99-00529V-10249 from the California Breast Cancer Research Program to M.K.. Fellowship support was by N.D. and E.H were supported by the Fondation pour la Recherche Medicale (N.D.) the Deutsche Forschungsgemeinschaft (E.H.), the Sontag Foundation Fellowship of the Arthritis National Research Foundation (M.D.), the California Breast Cancer Research Program (Y.C.), and the Cancer Research Institute (Z.L. and C.M.). We thank I. Verma, A. Beg, K. Pfeffer, N. Rice, and J. Hiscott for generously providing valuable cell lines, mice, or reagents. We thank T. Banks, S. Rickert, C. Benedict, S. Santee, and S. Granger for advice and helpful discussion. This is publication no. 491 from the La Jolla Institute for Allergy and Immunology.
PY - 2002/10/1
Y1 - 2002/10/1
N2 - The lymphotoxin-β receptor (LTβR) plays critical roles in inflammation and lymphoid organogenesis through activation of NF-κB. In addition to activation of the classical NF-κB, ligation of this receptor induces the processing of the cytosolic NF-κB2/p100 precursor to yield the mature p52 subunit, followed by translocation of p52 to the nucleus. This activation of NF-κB2 requires NIK and IKKα, while NEMO/IKKγ is dispensable for p100 processing. IKKβ-dependent activation of canonical NF-κB is required for the expression but not processing of p100 and for the expression of proinflammatory molecules including VCAM-1, MIP-1β, and MIP-2 in response to LTβR ligation. In contrast, IKKα controls the induction by LTβR ligation of chemokines and cytokines involved in lymphoid organogenesis, including SLC, BLC, ELC, SDF1, and BAFF.
AB - The lymphotoxin-β receptor (LTβR) plays critical roles in inflammation and lymphoid organogenesis through activation of NF-κB. In addition to activation of the classical NF-κB, ligation of this receptor induces the processing of the cytosolic NF-κB2/p100 precursor to yield the mature p52 subunit, followed by translocation of p52 to the nucleus. This activation of NF-κB2 requires NIK and IKKα, while NEMO/IKKγ is dispensable for p100 processing. IKKβ-dependent activation of canonical NF-κB is required for the expression but not processing of p100 and for the expression of proinflammatory molecules including VCAM-1, MIP-1β, and MIP-2 in response to LTβR ligation. In contrast, IKKα controls the induction by LTβR ligation of chemokines and cytokines involved in lymphoid organogenesis, including SLC, BLC, ELC, SDF1, and BAFF.
UR - http://www.scopus.com/inward/record.url?scp=18644380147&partnerID=8YFLogxK
U2 - 10.1016/S1074-7613(02)00423-5
DO - 10.1016/S1074-7613(02)00423-5
M3 - Article
C2 - 12387745
AN - SCOPUS:18644380147
SN - 1074-7613
VL - 17
SP - 525
EP - 535
JO - Immunity
JF - Immunity
IS - 4
ER -