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David L. Boone

Researcher at Indiana University

Publications -  60
Citations -  10165

David L. Boone is an academic researcher from Indiana University. The author has contributed to research in topics: Tumor necrosis factor alpha & ATG16L1. The author has an hindex of 26, co-authored 58 publications receiving 8916 citations. Previous affiliations of David L. Boone include University of Notre Dame & University of Chicago.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Failure to Regulate TNF-Induced NF-κB and Cell Death Responses in A20-Deficient Mice

TL;DR: A20 is critical for limiting inflammation by terminating TNF-induced NF-kappaB responses in vivo and is associated with severe inflammation and cachexia in mice deficient for A20.
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IL-15 receptor maintains lymphoid homeostasis by supporting lymphocyte homing and proliferation

TL;DR: IL-15Ralpha has pleiotropic roles in immune development and function, including the positive maintenance of lymphocyte homeostasis, and is generated in mice deficient in natural killer cells, natural killer T cells, CD8+ T lymphocytes, and TCRgammadelta intraepithelial lymphocytes.
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Interleukin 15 Is Required for Proliferative Renewal of Virus-specific Memory CD8 T Cells

TL;DR: Results show that IL-15 is not essential for the generation of memory CD8 T cells, but is required for homeostatic proliferation to maintain populations of memory cells over long periods of time.
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Interleukin (IL)-15Rα–deficient Natural Killer Cells Survive in Normal but Not IL-15Rα–deficient Mice

TL;DR: It is found that adoptive transfer of normal NK cells into mice lacking the high affinity interleukin (IL)-15 receptor, IL-15Rα, surprisingly results in the abrupt loss of these cells, and it is demonstrated that NK cell–independent IL- 15Rα expression is critical for maintaining peripheral NK cells, while IL-13R α expression on NK cells is not required for this function.