Research Topics
Genomes and Genes | Brian M J FoxwellSummaryAffiliation: Imperial College Country: UK Publications
| Collaborators
|
Detail Information
Publications
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...
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...- Tolerance induced via TLR2 and TLR4 in human dendritic cells: role of IRAK-1Valerie Albrecht
Helmholtz Center München, German Research Center for Environmental Health and Asklepios Fachkliniken Gauting, Inflammatory Lung Diseases, 82131 Gauting, Germany
BMC Immunol 9:69. 2008..We have analysed tolerance induced in human in-vitro generated DCs by repeated stimulation with ligands for TLR4 and TLR2... - Adenoviral transgene delivery provides an approach to identifying important molecular processes in inflammation: evidence for heterogenecity in the requirement for NFkappaB in tumour necrosis factor productionB M Foxwell
Kennedy Institute of Rheumatology Division, Imperial College School of Medicine, 1 Aspenlea Road, Hammersmith, London, UK
Ann Rheum Dis 59:i54-9. 2000.... - High efficiency gene transfer is an efficient way of defining therapeutic targets: a functional genomics approachB M Foxwell
Kennedy Institute of Rheumatology Division, Imperial College School of Medicine, London, UK
Ann Rheum Dis 60:iii13-7. 2001..Studying the intracellular signalling mechanism used by dendritic cells would provide an insight into the functioning of these cells and give clues to strategies for immunomodulation... - 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... - 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... - 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... 
Inhibitors of p38 suppress cytokine production in rheumatoid arthritis synovial membranes: does variable inhibition of interleukin-6 production limit effectiveness in vivo?Theresa H Page
Faculty of Medicine, Imperial College of Science, Technology and Medicine, London, UK
Arthritis Rheum 62:3221-31. 2010....- SIGIRR/TIR-8 is an inhibitor of Toll-like receptor signaling in primary human cells and regulates inflammation in models of rheumatoid arthritisStefan K Drexler
Imperial College London, London, UK
Arthritis Rheum 62:2249-61. 2010..Therefore, the purpose of this study was to investigate the involvement of SIGIRR in regulating inflammation in disease-relevant models... - 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... - RelB/p50 regulates CCL19 production, but fails to promote human DC maturationChiara Gasparini
Kennedy Institute of Rheumatology Division, School of Medicine, Imperial College London, London, UK
Eur J Immunol 39:2215-23. 2009..In conclusion, we demonstrated that RelB/p50 was active only in DC expressing both RelB and p50, and induced CCL19 production, but not DC maturation... - Nonsteroidal anti-inflammatory drugs increase TNF production in rheumatoid synovial membrane cultures and whole bloodTheresa H Page
The Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science, Technology and Medicine, London, United Kingdom
J Immunol 185:3694-701. 2010..Thus, by reducing the level of PGE(2), NSAIDs can increase TNF production and may exacerbate the proinflammatory environment both within the rheumatoid arthritis joint and the systemic environment... - 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... - 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... - 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... - 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... - 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... - 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.... - 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... - 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.... - 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... - Adenoviral targeting of signal transduction pathways in synovial cell culturesAlison Davis
Kennedy Institute of Rheumatology Division, Imperial College London, UK
Methods Mol Med 136:395-419. 2007..This is very important in studies of tissues such as rheumatoid synovium where sorting of cells will damage the biological value of the system... - 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... - 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... - Toll-like receptor-2 mediates inflammation and matrix degradation in human atherosclerosisClaudia Monaco
Kennedy Institute of Rheumatology Division, Imperial College, 65 Aspenlea Rd, London W6 8LH, UK
Circulation 120:2462-9. 2009..We explored the effects of blocking TLR-2, TLR-4, and myeloid differentiation primary response gene 88 (MyD88), a signaling adaptor shared by most TLRs and interleukin-1 receptor (IL-1R), in an in vitro model of human atherosclerosis... - 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 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... - 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... - 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.... - 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.... - 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...