Journal
IMMUNITY
Volume 17, Issue 4, Pages 525-535Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(02)00423-5
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Funding
- NCI NIH HHS [CA69381] Funding Source: Medline
- NIAID NIH HHS [AI43477, AI44828, AI48073, AI03368] Funding Source: Medline
- NIEHS NIH HHS [ES04151] Funding Source: Medline
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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.
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