B Foxwell

Summary

Affiliation: Imperial College
Country: UK

Publications

  1. pmc T-cell contact-dependent regulation of CC and CXC chemokine production in monocytes through differential involvement of NFkappaB: implications for rheumatoid arthritis
    Jonathan 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
  2. pmc Cell signalling in macrophages, the principal innate immune effector cells of rheumatoid arthritis
    Stefan 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
  3. ncbi Expression of constitutively active STAT3 can replicate the cytokine-suppressive activity of interleukin-10 in human primary macrophages
    Lynn 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
  4. pmc Prospects for the development of small molecular weight compounds to replace anti-tumour necrosis factor biological agents
    B 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
  5. ncbi Autocrine and paracrine regulation of human T cell IL-10 production
    S B Cohen
    Kennedy Institute of Rheumatology and The Anthony Nolan Bone Marrow Trust and the Department of Hematology, The Royal Free Hospital, London, United Kingdom
    J Immunol 158:5596-602. 1997
  6. ncbi Targeting intracellular mediators of pattern-recognition receptor signalling to adjuvant vaccination
    J Wales
    Kennedy Institute of Rheumatology, Imperial College London, 1 Aspenlea Road, London W6 8LH, U K
    Biochem Soc Trans 35:1501-3. 2007
  7. ncbi Bruton's tyrosine kinase is required for TLR2 and TLR4-induced TNF, but not IL-6, production
    Nicole 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
  8. ncbi Chemical inhibition of Src family kinases affects major LPS-activated pathways in primary human macrophages
    Maria 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
  9. ncbi IL-10 induces IL-10 in primary human monocyte-derived macrophages via the transcription factor Stat3
    Karl J Staples
    Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK
    J Immunol 178:4779-85. 2007
  10. ncbi Bmx tyrosine kinase regulates TLR4-induced IL-6 production in human macrophages independently of p38 MAPK and NFkapp}B activity
    Christine D Palmer
    Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College London, London, UK
    Blood 111:1781-8. 2008

Collaborators

Detail Information

Publications30

  1. pmc T-cell contact-dependent regulation of CC and CXC chemokine production in monocytes through differential involvement of NFkappaB: implications for rheumatoid arthritis
    Jonathan 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...
  2. pmc Cell signalling in macrophages, the principal innate immune effector cells of rheumatoid arthritis
    Stefan 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...
  3. ncbi Expression of constitutively active STAT3 can replicate the cytokine-suppressive activity of interleukin-10 in human primary macrophages
    Lynn 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...
  4. pmc Prospects for the development of small molecular weight compounds to replace anti-tumour necrosis factor biological agents
    B 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
  5. ncbi Autocrine and paracrine regulation of human T cell IL-10 production
    S B Cohen
    Kennedy Institute of Rheumatology and The Anthony Nolan Bone Marrow Trust and the Department of Hematology, The Royal Free Hospital, London, United Kingdom
    J Immunol 158:5596-602. 1997
    ....
  6. ncbi Targeting intracellular mediators of pattern-recognition receptor signalling to adjuvant vaccination
    J 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...
  7. ncbi Bruton's tyrosine kinase is required for TLR2 and TLR4-induced TNF, but not IL-6, production
    Nicole 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
    ....
  8. ncbi Chemical inhibition of Src family kinases affects major LPS-activated pathways in primary human macrophages
    Maria 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
    ....
  9. ncbi IL-10 induces IL-10 in primary human monocyte-derived macrophages via the transcription factor Stat3
    Karl 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...
  10. ncbi Bmx tyrosine kinase regulates TLR4-induced IL-6 production in human macrophages independently of p38 MAPK and NFkapp}B activity
    Christine 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...
  11. ncbi 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 arthritis
    Fionula 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...
  12. ncbi 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...
  13. ncbi Nuclear factor-kappaB activation in alveolar macrophages requires IkappaB kinase-beta, but not nuclear factor-kappaB inducing kinase
    Matthew 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...
  14. ncbi Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn's disease
    David A van Heel
    Intestinal Inflammation and Repair Group, Department of Gastroenterology, Imperial College London, UK
    Lancet 365:1794-6. 2005
    ....
  15. ncbi A novel mechanism for TNF-alpha regulation by p38 MAPK: involvement of NF-kappa B with implications for therapy in rheumatoid arthritis
    Jamie 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...
  16. ncbi TNFalpha-induced macrophage chemokine secretion is more dependent on NF-kappaB expression than lipopolysaccharides-induced macrophage chemokine secretion
    Cathleen J Ciesielski
    Kennedy Institute of Rheumatology Division, Imperial College Faculty of Medicine, London, GB
    Eur J Immunol 32:2037-45. 2002
    ....
  17. ncbi IL-4 regulation of p38 MAPK signalling is dependent on cell type
    Abigail E Hunt
    UCSF Cancer Center, 2340 Sutter Street, 94115, USA
    Cytokine 18:295-303. 2002
    ....
  18. pmc Bruton's tyrosine kinase is required for lipopolysaccharide-induced tumor necrosis factor alpha production
    Nicole 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
    ....
  19. ncbi 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
    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...
  20. doi Bmx regulates LPS-induced IL-6 and VEGF production via mRNA stability in rheumatoid synovial fibroblasts
    Christine 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...
  21. ncbi Heme oxygenase 1 expression induced by IL-10 requires STAT-3 and phosphoinositol-3 kinase and is inhibited by lipopolysaccharide
    Giuseppe 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...
  22. doi Rac mediates TNF-induced cytokine production via modulation of NF-kappaB
    Lynn 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...
  23. pmc Could toll-like receptors provide a missing link in chronic inflammation in rheumatoid arthritis? Lessons from a study on human rheumatoid tissue
    Sandra 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
    ....
  24. ncbi Cutting edge: A transcriptional repressor and corepressor induced by the STAT3-regulated anti-inflammatory signaling pathway
    Karim 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...
  25. ncbi 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-6
    Abdulmunem 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...
  26. ncbi Potential of rifamides to inhibit TNF-induced NF-kappaB activation
    Ali 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...
  27. pmc High-efficiency gene transfer into nontransformed cells: utility for studying gene regulation and analysis of potential therapeutic targets
    Nicole 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...
  28. pmc Interleukin-10 suppression of myeloid cell activation--a continuing puzzle
    Lynn 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...
  29. ncbi A late, prolonged activation of the phosphatidylinositol 3-kinase pathway is required for T cell proliferation
    Ferdinand 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...
  30. ncbi Inhibition of NF-kappa B and oxidative pathways in human dendritic cells by antioxidative vitamins generates regulatory T cells
    Peng 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...