Arthritis, Immunology, Rheumatoid arthritis, Tumor necrosis factor alpha and Cytokine are his primary areas of study. Richard O. Williams interconnects Inflammation, T cell, Blockade and Pathology in the investigation of issues within Arthritis. His Type II collagen, Synovial membrane, Pathogenesis, Proinflammatory cytokine and Interleukin 17 study are his primary interests in Immunology.
His Type II collagen study combines topics in areas such as C57BL/6 and Autoimmune disease. Within one scientific family, he focuses on topics pertaining to Antibody under Rheumatoid arthritis, and may sometimes address concerns connected to Immunotherapy. His work deals with themes such as Interleukin, Analgesic and Monoclonal antibody, which intersect with Tumor necrosis factor alpha.
Richard O. Williams focuses on Immunology, Arthritis, Rheumatoid arthritis, Tumor necrosis factor alpha and Inflammation. His research brings together the fields of Disease and Immunology. His studies in Arthritis integrate themes in fields like Proinflammatory cytokine, Monoclonal antibody, Pharmacology and Pathology.
His work in Rheumatoid arthritis addresses issues such as Psoriasis, which are connected to fields such as Ankylosing spondylitis. His Tumor necrosis factor alpha study integrates concerns from other disciplines, such as Alpha, Monoclonal, Blockade, Necrosis and Interleukin. His Cytokine research integrates issues from Pathogenesis and Synovial membrane.
Richard O. Williams mainly investigates Immunology, Arthritis, Inflammation, Rheumatoid arthritis and Immune system. His research combines Genetic association and Immunology. His Arthritis research includes themes of Regulatory T cell, Antibody, Biomarker and Dexamethasone.
His Inflammation research includes elements of Kynurenine pathway, Kynurenine, Cell, Cancer research and Pharmacology. The Rheumatoid arthritis study combines topics in areas such as Autoimmunity, Monoclonal antibody and Downregulation and upregulation. His Immune system research is multidisciplinary, incorporating perspectives in Proinflammatory cytokine, Autoimmune disease and Antigen.
The scientist’s investigation covers issues in Immunology, T cell, Arthritis, Inflammation and Immune system. Richard O. Williams studies Tumor necrosis factor alpha which is a part of Immunology. His research integrates issues of Receptor and Rheumatoid arthritis in his study of T cell.
His work investigates the relationship between Arthritis and topics such as Biomarker that intersect with problems in Kynurenine pathway, Neurodegeneration, Huntington's disease, Regulatory T cell and Kynurenine. As a part of the same scientific study, Richard O. Williams usually deals with the Inflammation, concentrating on Autoimmune disease and frequently concerns with DNA methylation, Tumor necrosis factor receptor 2, Phenotype, FOXP3 and Proinflammatory cytokine. His Immune system study combines topics in areas such as In vitro, Antibody, Arginine and Protein-Arginine Deiminases.
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Anti-tumor necrosis factor ameliorates joint disease in murine collagen-induced arthritis.
Richard O. Williams;Marc Feldmann;Ravinder N. Maini.
Proceedings of the National Academy of Sciences of the United States of America (1992)
Relationship between Th1/Th2 cytokine patterns and the arthritogenic response in collagen‐induced arthritis
Claudia Mauri;Richard O. Williams;Marita Walmsley;Marc Feldmann.
European Journal of Immunology (1996)
Interleukin-10 inhibition of the progression of established collagen-induced arthritis.
Marita Walmsley;Peter D. Katsikis;Erika Abney;Sarah Parry.
Arthritis & Rheumatism (1996)
Monoclonal anti-TNF alpha antibody as a probe of pathogenesis and therapy of rheumatoid disease.
Ravinder N. Maini;Michael J. Elliott;Fionula M. Brennan;Richard O. Williams.
Immunological Reviews (1995)
Synergy between anti-CD4 and anti-tumor necrosis factor in the amelioration of established collagen-induced arthritis.
Richard O. Williams;Lesley J. Mason;Marc Feldmann;Ravinder N. Maini.
Proceedings of the National Academy of Sciences of the United States of America (1994)
RHAMM, a receptor for hyaluronan-mediated motility, compensates for CD44 in inflamed CD44-knockout mice: A different interpretation of redundancy
Shlomo Nedvetzki;Erez Gonen;Nathalie Assayag;Reuven Reich.
Proceedings of the National Academy of Sciences of the United States of America (2004)
Blockade of tumor necrosis factor in collagen-induced arthritis reveals a novel immunoregulatory pathway for Th1 and Th17 cells
Clare A. Notley;Julia J. Inglis;Saba Alzabin;Fiona E. McCann.
Journal of Experimental Medicine (2008)
Effects of fluoxetine on functional outcomes after acute stroke (FOCUS): a pragmatic, double-blind, randomised, controlled trial
Martin Dennis;Gillian Mead;John Forbes;Catriona Graham.
The Lancet (2019)
IFN-λ resolves inflammation via suppression of neutrophil infiltration and IL-1β production
Katrina Blazek;Hayley L. Eames;Miriam Weiss;Adam J. Byrne.
Journal of Experimental Medicine (2015)
Fluoxetine and citalopram exhibit potent antiinflammatory activity in human and murine models of rheumatoid arthritis and inhibit toll‐like receptors
Sandra M. Sacre;Mino Medghalchi;Bernard Gregory;Fionula Brennan.
Arthritis & Rheumatism (2010)
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