2011
DOI: 10.1016/j.cytogfr.2011.11.007
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Biology and signal transduction pathways of the Lymphotoxin-αβ/LTβR system

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Cited by 61 publications
(56 citation statements)
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“…The latter is triggered by either binding of LTα1β2 heterotrimers expressed by activated T, B, natural killer (NK) cells and lymphoid tissue inducer cells, or LIGHT (homologous to l ymphotoxin exhibits i nducible expression and competes with HSV g lycoprotein D for binding to h erpes virus entry mediator, a receptor expressed on T lymphocytes), a TNFSF member expressed on T lymphocytes 9–11. Under pathological conditions, LTs and LIGHT can also be expressed by epithelial cells 12 13. LTβR is mainly expressed on epithelial and stromal cells, thereby enabling the communication with lymphocytes.…”
Section: Introductionmentioning
confidence: 99%
“…The latter is triggered by either binding of LTα1β2 heterotrimers expressed by activated T, B, natural killer (NK) cells and lymphoid tissue inducer cells, or LIGHT (homologous to l ymphotoxin exhibits i nducible expression and competes with HSV g lycoprotein D for binding to h erpes virus entry mediator, a receptor expressed on T lymphocytes), a TNFSF member expressed on T lymphocytes 9–11. Under pathological conditions, LTs and LIGHT can also be expressed by epithelial cells 12 13. LTβR is mainly expressed on epithelial and stromal cells, thereby enabling the communication with lymphocytes.…”
Section: Introductionmentioning
confidence: 99%
“…This triggers the activation of the inhibitor of ĸB (IĸB) kinase (IKK) complex (consisting of IKKα, IKKβ, and NEMO/IKKβ) by ubiquitination of the regulatory subunit NEMO leading to phosphorylation of IKKβ. IKKβ then in turn leads to the phosphorylation and proteasomal degradation of IĸBa, hence allowing nuclear translocation of the p50/RelA (NF-ĸB1) heterodimer mediating proinflammatory and prosurvival signaling [33]. …”
Section: Physiologymentioning
confidence: 99%
“…Most of these cytokines are involved in the regulation of several steps of the biological processes related to inflammatory and immune responses. 84,85 Extensive preclinical and clinical investigations have shown that TNF has a pivotal role in the pathogenesis and pathophysiology of IMDs, which has been confirmed by the efficacy of anti-TNF biotechnological drugs, such as etanercept, infliximab and adalimumab, in the therapeutic management of these disorders. 2,86 Overexpression of TNF has been shown to promote proinflammatory processes.…”
Section: Th17 Pathwaymentioning
confidence: 96%