2013 - Member of the National Academy of Sciences
2009 - Fellow of the Royal Society, United Kingdom
2001 - Gottschalk Medal, Australian Academy of Science
1998 - AAI-BD Biosciences Investigator Award, American Association of Immunologists
His main research concerns Antigen, Immunology, Cell biology, Molecular biology and B cell. Christopher C. Goodnow interconnects Receptor, Antibody and B-cell receptor, Receptor editing in the investigation of issues within Antigen. His Cell biology study incorporates themes from Central tolerance, Cellular differentiation, Lymphocyte and Bone marrow.
His work deals with themes such as RNA, T cell, Clonal deletion, Gene silencing and Ubiquitin ligase, which intersect with Molecular biology. His B cell study integrates concerns from other disciplines, such as Adoptive cell transfer and CD40, B-1 cell. His Immune tolerance research is multidisciplinary, incorporating perspectives in Clonal anergy, Signal transduction, Transgene and Self Tolerance.
His primary scientific interests are in Cell biology, Immunology, Antigen, Molecular biology and B cell. His work carried out in the field of Cell biology brings together such families of science as Cytotoxic T cell, Cell and CD8. His study involves Immune system, Autoimmunity, Autoantibody, Germinal center and Autoimmune disease, a branch of Immunology.
His study focuses on the intersection of Antigen and fields such as Antibody with connections in the field of Genetically modified mouse. His research integrates issues of T cell, T-cell receptor, Naive B cell and Mutant in his study of Molecular biology. His research in B cell intersects with topics in Lymphocyte, Immunoglobulin M and CD40, B-1 cell.
Cell biology, B cell, Antibody, Molecular biology and Immune system are his primary areas of study. His Cell biology research is multidisciplinary, relying on both Cell, Transcription factor, Germinal center, Antigen and Cytotoxic T cell. His B cell research is classified as research in Immunology.
His research investigates the connection between Antibody and topics such as Mutation that intersect with issues in Affinity maturation, Allele, CD19 and Carcinogenesis. The various areas that Christopher C. Goodnow examines in his Molecular biology study include Missense mutation, Mutant, Immune tolerance, Peripheral blood mononuclear cell and B-cell receptor. Genetics covers Christopher C. Goodnow research in Immune system.
The scientist’s investigation covers issues in Cell biology, Mutation, Cell growth, Germinal center and Transcription factor. He has researched Cell biology in several fields, including Cell, Inflammasome and Interferon regulatory factors. His Mutation study combines topics in areas such as Acquired immune system, Immune system, Antibody and Somatic hypermutation.
His Antibody research includes elements of Germline mutation and Virology. His Germinal center research is multidisciplinary, incorporating elements of Epitope, Affinity maturation, Antigen, Cytotoxic T cell and Self Tolerance. The concepts of his Transcription factor study are interwoven with issues in Pyroptosis, Mucosal associated invariant T cell, Cellular differentiation, Signaling lymphocytic activation molecule and Transcriptome.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Differential activation of transcription factors induced by Ca2+ response amplitude and duration
Ricardo E. Dolmetsch;Richard S. Lewis;Christopher C. Goodnow;James I. Healy.
Nature (1997)
Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
Nobuhiko Kayagaki;Irma B. Stowe;Bettina L. Lee;Karen O’Rourke.
Nature (2015)
C3d of Complement as a Molecular Adjuvant: Bridging Innate and Acquired Immunity
Paul W. Dempsey;Michael E. D. Allison;Srinivas Akkaraju;Christopher C. Goodnow.
Science (1996)
Aire regulates negative selection of organ-specific T cells
Adrian Liston;Sylvie Lesage;Judith Wilson;Leena Peltonen.
Nature Immunology (2003)
A RING-type ubiquitin ligase family member required to repress follicular helper T cells and autoimmunity
Carola G. Vinuesa;Matthew C. Cook;Constanza Angelucci;Vicki Athanasopoulos.
Nature (2005)
Elimination from peripheral lymphoid tissues of self-reactive B lymphocytes recognizing membrane-bound antigens.
Suzanne B. Hartley;Jeffrey Crosbie;Robert Brink;Aaron B. Kantor.
Nature (1991)
Cellular and genetic mechanisms of self tolerance and autoimmunity
Christopher C. Goodnow;Jonathon Sprent;Barbara Fazekas de St Groth;Carola G. Vinuesa.
Nature (2005)
Expansion of circulating T cells resembling follicular helper T cells is a fixed phenotype that identifies a subset of severe systemic lupus erythematosus.
Nicholas Simpson;Paul A. Gatenby;Anastasia Wilson;Shreya Malik.
Arthritis & Rheumatism (2010)
Aberrant mucin assembly in mice causes endoplasmic reticulum stress and spontaneous inflammation resembling ulcerative colitis.
Chad K Heazlewood;Matthew C Cook;Rajaraman Eri;Gareth R Price.
PLOS Medicine (2008)
Elimination of self-reactive B lymphocytes proceeds in two stages: Arrested development and cell death
Suzanne B. Hartley;Michael P. Cooke;David A. Fulcher;Alan W. Harris.
Cell (1993)
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