C
Clive Smith
Researcher at Imperial College London
Publications - 17
Citations - 992
Clive Smith is an academic researcher from Imperial College London. The author has contributed to research in topics: Cytokine & Tumor necrosis factor alpha. The author has an hindex of 12, co-authored 17 publications receiving 961 citations. Previous affiliations of Clive Smith include Charing Cross Hospital.
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Journal ArticleDOI
Functional consequences of a polymorphism affecting NF-kappaB p50-p50 binding to the TNF promoter region.
Irina A. Udalova,Anna Richardson,Agnes Denys,Clive Smith,Hans Ackerman,Brian M. J. Foxwell,Dominic P. Kwiatkowski +6 more
TL;DR: Using an adenoviral reporter assay, the variant which binds p50-p50 results in a reduction of lipopolysaccharide-inducible gene expression in primary human monocytes and illustrates the potential for genetic modulation of inflammatory gene regulation in humans by subtle nucleotide changes that alter the relative binding affinities of different forms of the NF-κB complex.
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Distinct pathways of LPS-induced NF-kappa B activation and cytokine production in human myeloid and nonmyeloid cells defined by selective utilization of MyD88 and Mal/TIRAP
Evangelos Andreakos,Sandra Sacre,Clive Smith,Anna M. Lundberg,Serafim Kiriakidis,Tim Stonehouse,Claudia Monaco,Marc Feldmann,Brian M. J. Foxwell +8 more
TL;DR: It is found that MyD88 and Mal/TIRAP are essential for LPS-induced I kappa B alpha phosphorylation, NF-kappa B activation, and interleukin 6 (IL-6) or IL-8 production in fibroblasts and endothelial cells in a pathway that also requires IKK2.
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Evidence for a dual mechanism for IL-10 suppression of TNF-alpha production that does not involve inhibition of p38 mitogen-activated protein kinase or NF-kappa B in primary human macrophages.
Agnes Denys,Irina A. Udalova,Clive Smith,Lynn M. Williams,Cathleen J. Ciesielski,Jamie Campbell,Caroline Andrews,Dominic Kwaitkowski,Brian M. J. Foxwell +8 more
TL;DR: To the authors' knowledge, this is the first time that a dual mechanism for IL-10 function has been demonstrated and may explain the diversity previously ascribed to the complex mechanisms ofIL-10 anti-inflammatory activity.
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Is NF-kappaB a useful therapeutic target in rheumatoid arthritis?
Marc Feldmann,Evangelos Andreakos,Clive Smith,Jan Bondeson,Satomichi Yoshimura,Serafim Kiriakidis,Claudia Monaco,C Gasparini,Sandra Sacre,Anna M. Lundberg,Ewa M. Paleolog,Nicole J. Horwood,Fionula M. Brennan,Brian M. J. Foxwell +13 more
TL;DR: The effects of NF-κB blockade in rheumatoid arthritis, inflammation and immunity, and consider possible therapeutic targets within the NF-σκB family are discussed.
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NF-kappaB-inducing kinase is dispensable for activation of NF-kappaB in inflammatory settings but essential for lymphotoxin beta receptor activation of NF-kappaB in primary human fibroblasts.
Clive Smith,Evangelos Andreakos,James B. Crawley,Fionula M. Brennan,Marc Feldmann,Brian M. J. Foxwell +5 more
TL;DR: Investigation of the role of NIK in LPS, IL-1, TNF-α, and lymphotoxin (LT) βR signaling in primary human cells and T NF-α expression from rheumatoid tissue shows that, in the primary systems tested, NIK has a restricted role in LTβR signaling and is not required by the other stimuli tested.