O
Odilia B. J. Corneth
Researcher at Erasmus University Rotterdam
Publications - 44
Citations - 1275
Odilia B. J. Corneth is an academic researcher from Erasmus University Rotterdam. The author has contributed to research in topics: Bruton's tyrosine kinase & B cell. The author has an hindex of 15, co-authored 37 publications receiving 892 citations. Previous affiliations of Odilia B. J. Corneth include Erasmus University Medical Center & University Medical Center.
Papers
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Journal ArticleDOI
Btk levels set the threshold for B-cell activation and negative selection of autoreactive B cells in mice
Laurens P. Kil,Marjolein J. W. de Bruijn,Menno van Nimwegen,Odilia B. J. Corneth,Jan Piet van Hamburg,Gemma M. Dingjan,Friedrich Thaiss,Guus F. Rimmelzwaan,Dirk Elewaut,Dianne Delsing,Pieter Fokko van Loo,Rudi W. Hendriks +11 more
TL;DR: Transgenic mice overexpressing Btk specifically in B cells spontaneously formed germinal centers and manifested increased plasma cell numbers, leading to antinuclear autoantibody production and systemic lupus erythematosus (SLE)-like autoimmune pathology affecting kidneys, lungs, and salivary glands.
Journal ArticleDOI
Attenuation of Follicular Helper T Cell-Dependent B Cell Hyperactivity by Abatacept Treatment in Primary Sjogren's Syndrome
Gwenny M Verstappen,Petra M. Meiners,Odilia B. J. Corneth,Annie Visser,Suzanne Arends,Wayel H. Abdulahad,Rudi W. Hendriks,Arjan Vissink,Frans G. M. Kroese,Hendrika Bootsma +9 more
TL;DR: The aim is to assess the effect of abatacept (CTLA‐4Ig), which limits T cell activation, on homeostasis of CD4+ T cell subsets and T cell–dependent B cell hyperactivity in patients with primary Sjögren's syndrome.
Journal ArticleDOI
Th17 cells in primary Sjogren's syndrome : Pathogenicity and plasticity
TL;DR: It is postulate that plasticity towards Th17.1 cells in pSS may enhance pathogenicity of Th17 cells at the main target sites of the disease, i.e. salivary and lacrimal glands.
Book ChapterDOI
BTK Signaling in B Cell Differentiation and Autoimmunity
TL;DR: The role of BTK during B cell differentiation in vivo is focused on, both in the regulation of expansion and in the developmental progression of pre-B cells in the bone marrow and as a crucial signal transducer of signals downstream of the IgM or IgG B cell antigen receptor (BCR) in mature B cells governing proliferation, survival, and differentiation.
Journal ArticleDOI
The Role of Bruton's Tyrosine Kinase in Immune Cell Signaling and Systemic Autoimmunity.
TL;DR: Interestingly, increased BTK protein expression in patients with systemic autoimmune disease appears to be correlated with autoantibody production, and BTK may promote autoimmunity as an important driver of an imbalance in B-T cell interaction.