Research Topics
Species | B FoxwellSummaryAffiliation: Imperial College Country: UK Publications
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Detail Information
Publications
T-cell contact-dependent regulation of CC and CXC chemokine production in monocytes through differential involvement of NFkappaB: implications for rheumatoid arthritisJonathan T Beech
Kennedy Institute of Rheumatology Division, Imperial College School of Medicine, 1 Aspenlea Road, Hammersmith, London W6 8LH, UK
Arthritis Res Ther 8:R168. 2006..Moreover, this study provides further evidence that cytokine-activated T cells share aspects of their effector function with RA synovial T cells and that their targeting in the clinic has therapeutic potential...- Cell signalling in macrophages, the principal innate immune effector cells of rheumatoid arthritisStefan K Drexler
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science, Technology and Medicine, 65 Aspenlea Road, Hammersmith, London, W6 8LH, UK
Arthritis Res Ther 10:216. 2008..This review will concentrate on the role of signalling pathways in innate immune cells in the context of rheumatoid arthritis... 
Expression of constitutively active STAT3 can replicate the cytokine-suppressive activity of interleukin-10 in human primary macrophagesLynn M Williams
Kennedy Institute of Rheumatology Division, Imperial College London, ARC Building, 1 Aspenlea Road, London W6 8LH, United Kingdom
J Biol Chem 282:6965-75. 2007..However, in synovial fibroblasts, STAT3 did not suppress IL-6 production, suggesting that the cellular environment plays an important role in dictating whether STAT3 drives a pro- or anti-inflammatory response...- Prospects for the development of small molecular weight compounds to replace anti-tumour necrosis factor biological agentsB Foxwell
The Kennedy Institute of Rheumatology Division, Imperial College London, The Charing Cross Campus, ARC Building, 1 Aspenlea Road, London W6 8LH, UK
Ann Rheum Dis 62:ii90-3. 2003 - Targeting intracellular mediators of pattern-recognition receptor signalling to adjuvant vaccinationJ Wales
Kennedy Institute of Rheumatology, Imperial College London, 1 Aspenlea Road, London W6 8LH, U K
Biochem Soc Trans 35:1501-3. 2007..The targeting of PRR intracellular signalling networks would allow for greater specificity and reduced systemic toxicity. The present review examines the successes seen with overexpression or repression of PRR signalling molecules... - Anti-TNF therapy: where have we got to in 2005?Marc Feldmann
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College, 1 Aspenlea Road, London W6 8LH, UK
J Autoimmun 25:26-8. 2005..There are still many limitations, but the prospects for the future are intriguing... - Bruton's tyrosine kinase is required for TLR2 and TLR4-induced TNF, but not IL-6, productionNicole J Horwood
Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Charing Cross Campus, 1 Aspenlea Road, London W6 8LH, United Kingdom
J Immunol 176:3635-41. 2006.... - IL-10 induces IL-10 in primary human monocyte-derived macrophages via the transcription factor Stat3Karl J Staples
Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK
J Immunol 178:4779-85. 2007..These data show that IL-10 induces IL-10 in monocyte-derived macrophages in an autocrine manner via activation of the transcription factor Stat3... - Chemical inhibition of Src family kinases affects major LPS-activated pathways in primary human macrophagesMaria J Smolinska
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Charing Cross Campus, ARC Building, 1 Aspenlea Road, London W6 8LH, UK
Mol Immunol 45:990-1000. 2008.... - Could toll-like receptors provide a missing link in chronic inflammation in rheumatoid arthritis? Lessons from a study on human rheumatoid tissueSandra M Sacre
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College London, 1 Aspenlea Road, Hammersmith, London W6 8LH, UK
Ann Rheum Dis 66:iii81-6. 2007.... - Bmx tyrosine kinase regulates TLR4-induced IL-6 production in human macrophages independently of p38 MAPK and NFkapp}B activityChristine D Palmer
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College London, London, UK
Blood 111:1781-8. 2008..These data have important implications for the design of therapeutics targeted against specific cytokines and their regulators in inflammatory disease... 
Rac mediates TNF-induced cytokine production via modulation of NF-kappaBLynn M Williams
Kennedy Institute of Rheumatology Division, Imperial College London, Hammersmith, London W6 8LH, United Kingdom
Mol Immunol 45:2446-54. 2008..This would suggest that TNF-induced activation of Rac, lies upstream of NF-kappaB activation, and that the inhibition of this pathway results in inhibition of cytokine production...- Bmx regulates LPS-induced IL-6 and VEGF production via mRNA stability in rheumatoid synovial fibroblastsChristine D Palmer
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College London, Charing Cross Campus, ARC Building, 65 Aspenlea Road, London W6 8LH, UK
Biochem Biophys Res Commun 370:599-602. 2008..This is an important insight into the regulation of VEGF, which is involved in a wide range of different pathologies, and may lead to more effective design of novel anti-inflammatory/angiogenic therapeutics for conditions such as RA... - Evidence that rheumatoid arthritis synovial T cells are similar to cytokine-activated T cells: involvement of phosphatidylinositol 3-kinase and nuclear factor kappaB pathways in tumor necrosis factor alpha production in rheumatoid arthritisFionula M Brennan
Chester Beatty Laboratories, Institute of Cancer Research, London, UK
Arthritis Rheum 46:31-41. 2002..To investigate the mechanism that leads to the spontaneous production of tumor necrosis factor alpha (TNFalpha) in rheumatoid arthritis (RA) synovial tissue... - Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn's diseaseDavid A van Heel
Intestinal Inflammation and Repair Group, Department of Gastroenterology, Imperial College London, UK
Lancet 365:1794-6. 2005.... - Nuclear factor-kappaB activation in alveolar macrophages requires IkappaB kinase-beta, but not nuclear factor-kappaB inducing kinaseMatthew Conron
Kennedy Institute of Rheumatology, Hammersmith, London, United Kingdom
Am J Respir Crit Care Med 165:996-1004. 2002..We observed that IKKbeta, but not NIK, was required for NF-kappaB activation. The results of this study identify IKKbeta, but not NIK, as a potential therapeutic target in diseases that involve NF-kappaB-dependent gene transcription... - 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 macrophagesAgnes Denys
Kennedy Institute of Rheumatology Division, Imperial College Faculty of Medicine, Charing Cross Campus, 1 Aspenlea Road, London, United Kingdom
J Immunol 168:4837-45. 2002..Overall, these results may explain the diversity previously ascribed to the complex mechanisms of IL-10 anti-inflammatory activity... - TNFalpha-induced macrophage chemokine secretion is more dependent on NF-kappaB expression than lipopolysaccharides-induced macrophage chemokine secretionCathleen J Ciesielski
Kennedy Institute of Rheumatology Division, Imperial College Faculty of Medicine, London, GB
Eur J Immunol 32:2037-45. 2002.... - IL-4 regulation of p38 MAPK signalling is dependent on cell typeAbigail E Hunt
UCSF Cancer Center, 2340 Sutter Street, 94115, USA
Cytokine 18:295-303. 2002.... - Bruton's tyrosine kinase is required for lipopolysaccharide-induced tumor necrosis factor alpha productionNicole J Horwood
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science, Technology and Medicine, London W6 8LH, United Kingdom
J Exp Med 197:1603-11. 2003.... - Heme oxygenase 1 expression induced by IL-10 requires STAT-3 and phosphoinositol-3 kinase and is inhibited by lipopolysaccharideGiuseppe A Ricchetti
Kennedy Institute of Rheumatology Division, Imperial College London, Hammersmith, UK
J Leukoc Biol 76:719-26. 2004..In summary, although IL-10 does regulate HO-1 expression, it does not appear to play a significant role in the anti-inflammatory activity of the cytokine... - A novel mechanism for TNF-alpha regulation by p38 MAPK: involvement of NF-kappa B with implications for therapy in rheumatoid arthritisJamie Campbell
Kennedy Institute of Rheumatology Division, Imperial College School of Medicine Hammersmith, London, United Kingdom
J Immunol 173:6928-37. 2004..These results indicate despite disappointing results with p38 MAPK inhibitors in the clinic, this kinase is a valid target in rheumatoid disease... - Inhibition of p38 mitogen-activated protein kinase is effective in the treatment of experimental crescentic glomerulonephritis and suppresses monocyte chemoattractant protein-1 but not IL-1beta or IL-6Abdulmunem Sheryanna
Renal Section, Division of Medicine, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 ONN, UK
J Am Soc Nephrol 18:1167-79. 2007..Therefore, p38 MAPK therapeutic blockade is a promising strategy in the treatment of antibody-mediated glomerulonephritis... - A late, prolonged activation of the phosphatidylinositol 3-kinase pathway is required for T cell proliferationFerdinand V Lali
Kennedy Institute of Rheumatology Division, Imperial College London, UK
J Immunol 172:3527-34. 2004..The data presented here will have major implications for our understanding of the mechanism of T cell proliferation as well as the regulation of PI 3-K activity... - High-efficiency gene transfer into nontransformed cells: utility for studying gene regulation and analysis of potential therapeutic targetsNicole J Horwood
Kennedy Institute of Rheumatology Division, Imperial College Faculty of Medicine, London, UK
Arthritis Res 4:S215-25. 2002..While the NF-kappaB pathway has proven to be a major mediator of tumour necrosis factor alpha production, it is not exclusive and work evaluating the involvement of other pathways is ongoing... - Cutting edge: A transcriptional repressor and corepressor induced by the STAT3-regulated anti-inflammatory signaling pathwayKarim C El Kasmi
Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
J Immunol 179:7215-9. 2007..Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10... - Interleukin-10 suppression of myeloid cell activation--a continuing puzzleLynn M Williams
The Kennedy Institute of Rheumatology Division, Imperial College, London, UK
Immunology 113:281-92. 2004..Here we would like to highlight novel findings and discuss their implications in the context of current understanding of IL-10 signalling... - Potential of rifamides to inhibit TNF-induced NF-kappaB activationAli A Pahlevan
Infectious Diseases and Microbiology, Charing Cross Campus, Imperial College, London, UK
J Antimicrob Chemother 49:531-4. 2002..As TNF is important in the host defence against tuberculosis, suppression of this activity may provide a potential mechanism of rifamide immunosuppressive activity... - Inhibition of NF-kappa B and oxidative pathways in human dendritic cells by antioxidative vitamins generates regulatory T cellsPeng H Tan
Department of Immunology, Division of Medicine, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom
J Immunol 174:7633-44. 2005..These data indicate that vitamin C- and E-treated DC might be useful for the induction of tolerance to allo- or autoantigens...