Danyal Butt
Garvan Institute of Medical Research
2 Papers
Danyal Butt is an academic researcher from Garvan Institute of Medical Research. The author has contributed to research in topics: Biology & Somatic hypermutation. The author has an hindex of 2, co-authored 2 publications. Previous affiliations of Danyal Butt include University of New South Wales.
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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.
FAS Inactivation Releases Unconventional Germinal Center B Cells that Escape Antigen Control and Drive IgE and Autoantibody Production.
Danyal Butt,Danyal Butt,Tyani D. Chan,Tyani D. Chan,Katherine Bourne,Jana R. Hermes,Akira Nguyen,Aaron L. Statham,Lorraine A. O'Reilly,Lorraine A. O'Reilly,Andreas Strasser,Andreas Strasser,Susan Price,Peter R. Schofield,Daniel Christ,Daniel Christ,Antony Basten,Antony Basten,Cindy S. Ma,Cindy S. Ma,Stuart G. Tangye,Stuart G. Tangye,Tri Giang Phan,Tri Giang Phan,V. Koneti Rao,Robert Brink,Robert Brink +26 more
TL;DR: It is shown that FAS is in fact not required for this process, and instead, FAS inactivation led to accumulation of a population of unconventional GC B cells that underwent somatic hypermutation, survived despite losing antigen reactivity, and differentiated into a large population of plasma cells that included autoantibody-secreting clones.
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