Anthony Lau
Garvan Institute of Medical Research
8 Papers
Anthony Lau is an academic researcher from Garvan Institute of Medical Research. The author has contributed to research in topics: Immune system & Biology. The author has an hindex of 7, co-authored 8 publications. Previous affiliations of Anthony Lau include University of New South Wales & University of Bath.
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Papers
Germline-activating mutations in PIK3CD compromise B cell development and function.
Danielle T. Avery,Alisa Kane,Tina Nguyen,Tina Nguyen,Anthony Lau,Anthony Lau,Akira Nguyen,Akira Nguyen,Helen Lenthall,Kathryn Payne,Wei Shi,Wei Shi,Henry Brigden,Elise French,Julia Bier,Julia Bier,Jana R. Hermes,David Zahra,William A. Sewell,William A. Sewell,William A. Sewell,Danyal Butt,Danyal Butt,Michael Elliott,Michael Elliott,Kaan Boztug,Kaan Boztug,Isabelle Meyts,Sharon Choo,Peter Hsu,Melanie Wong,Lucinda J. Berglund,Lucinda J. Berglund,Paul Gray,Michael O'Sullivan,Theresa Cole,Steven M. Holland,Cindy S. Ma,Cindy S. Ma,Christoph Burkhart,Lynn M. Corcoran,Lynn M. Corcoran,Tri Giang Phan,Tri Giang Phan,Robert Brink,Robert Brink,Gulbu Uzel,Elissa K. Deenick,Elissa K. Deenick,Stuart G. Tangye,Stuart G. Tangye +50 more
TL;DR: Key roles for balanced PI3K signaling in B cell development and long-lived humoral immunity and memory are revealed and the validity of treating affected individuals with p110&dgr; inhibitors is established.
Activating mutations in PIK3CD disrupt the differentiation and function of human and murine CD4+ T cells.
Julia Bier,Julia Bier,Geetha Rao,Kathryn Payne,Henry Brigden,Henry Brigden,Elise French,Elise French,Simon J. Pelham,Simon J. Pelham,Anthony Lau,Anthony Lau,Helen Lenthall,Emily S.J. Edwards,Emily S.J. Edwards,Joanne Smart,Theresa Cole,Sharon Choo,Avni Y. Joshi,Roshini S. Abraham,Roshini S. Abraham,Michael O'Sullivan,Kaan Boztug,Kaan Boztug,Isabelle Meyts,Paul Gray,Lucinda J. Berglund,Lucinda J. Berglund,Peter Hsu,Peter Hsu,Melanie Wong,Melanie Wong,Steven M. Holland,Luigi D. Notarangelo,Gulbu Uzel,Cindy S. Ma,Cindy S. Ma,Robert Brink,Robert Brink,Stuart G. Tangye,Stuart G. Tangye,Elissa K. Deenick,Elissa K. Deenick +42 more
TL;DR: It is revealed that CD4+ T cells with overactive PI3K have aberrant activation and differentiation, thereby providing mechanistic insight into dysfunctional antibody responses in patients with PIK3CD GOF mutations.
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Activated PI3Kδ breaches multiple B cell tolerance checkpoints and causes autoantibody production
Anthony Lau,Anthony Lau,Danielle T. Avery,Katherine J. L. Jackson,Helen Lenthall,Stefano Volpi,Henry Brigden,Amanda J. Russell,Julia Bier,Julia Bier,Joanne H. Reed,Joanne H. Reed,Joanne Smart,Theresa Cole,Sharon Choo,Paul Gray,Lucinda J. Berglund,Lucinda J. Berglund,Peter Hsu,Melanie Wong,Michael O'Sullivan,Kaan Boztug,Isabelle Meyts,Gulbu Uzel,Luigi D. Notarangelo,Robert Brink,Robert Brink,Christopher C. Goodnow,Christopher C. Goodnow,Stuart G. Tangye,Stuart G. Tangye,Elissa K. Deenick,Elissa K. Deenick +32 more
TL;DR: In patients, gain-of-function (GOF) mutations in PIK3CD break tolerance, causing highly penetrant secretion of autoreactive IgM, and mouse models reveal that Pik3cd GOF subverts the response to self-antigen, preventing the induction of anergy and instead stimulating plasmablast and GC formation.
Molecular and cellular mechanisms underlying defective antibody responses
Elissa K. Deenick,Elissa K. Deenick,Anthony Lau,Anthony Lau,Julia Bier,Julia Bier,Alisa Kane +6 more
TL;DR: The molecular and cellular mechanisms of these rare monogenic conditions that disrupt antibody production are explored, which also have implications for understanding the causes of more common polygenic immune dysfunction.
Immune Dysregulation and Disease Pathogenesis due to Activating Mutations in PIK3CD —the Goldilocks’ Effect
Stuart G. Tangye,Stuart G. Tangye,Julia Bier,Julia Bier,Anthony Lau,Anthony Lau,Tina Nguyen,Tina Nguyen,Gulbu Uzel,Elissa K. Deenick,Elissa K. Deenick +10 more
TL;DR: Detailed analyses of patients with germline activating mutations in PIK3CD, as well as the parallel generation of novel murine models of this disease, have shed substantial light on the role of PI3K in lymphocyte development and differentiation, and mechanisms of disease pathogenesis resulting not only from Pik3CD mutations but genetic lesions in other components of thePI3K pathway.