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Barry R. Bloom
Researcher at Harvard University
Publications - 459
Citations - 59040
Barry R. Bloom is an academic researcher from Harvard University. The author has contributed to research in topics: Antigen & Mycobacterium tuberculosis. The author has an hindex of 116, co-authored 456 publications receiving 57021 citations. Previous affiliations of Barry R. Bloom include University of Würzburg & University of Genoa.
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Journal ArticleDOI
Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response
Philip T. Liu,Steffen Stenger,Huiying Li,Linda Wenzel,Belinda H. Tan,Stephan R. Krutzik,Maria Teresa Ochoa,Jürgen Schauber,Kent Wu,Christoph Meinken,Diane L. Kamen,Manfred Wagner,Robert Bals,Andreas Steinmeyer,Ulrich Zügel,Richard L. Gallo,David Eisenberg,Martin Hewison,Bruce W. Hollis,John S. Adams,Barry R. Bloom,Robert L. Modlin +21 more
TL;DR: The data support a link between TLRs and vitamin D–mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection.
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An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection.
JoAnne L. Flynn,John Chan,Karla J. Triebold,Dyana K. Dalton,Timothy A. Stewart,Barry R. Bloom +5 more
TL;DR: Gko mice have been developed which fail to produce IFN-gamma (gko), because of a targeted disruption of the gene for IFNs, and succumb to a rapid and fatal course of tuberculosis that could be delayed, but not prevented, by treatment with exogenous recombinant IFN.
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Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors.
Hans Brightbill,Daniel H. Libraty,Stephan R. Krutzik,Ruey-Bing Yang,John T. Belisle,Joshua R. Bleharski,Michael Maitland,Michael V. Norgard,Scott E. Plevy,Stephen T. Smale,Patrick J. Brennan,Barry R. Bloom,Barry R. Bloom,Paul J. Godowski,Robert L. Modlin +14 more
TL;DR: It is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs), and that Activation of TLRs by microbes may initiate innate defense mechanisms against infectious pathogens.
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Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice
JoAnne L. Flynn,Marsha M. Goldstein,John Chan,Karla J. Triebold,Klaus Pfeffer,Charles J. Lowenstein,Robert Schrelber,Tak W. Mak,Barry R. Bloom +8 more
TL;DR: The data from both models established that TNF alpha and the 55 kDa TNF receptor are essential for protection against tuberculosis in mice, and for reactive nitrogen production by macrophages early in infection.
Journal ArticleDOI
Mechanism of a Reaction in Vitro Associated with Delayed-Type Hypersensitivity
Barry R. Bloom,Boyce Bennett +1 more
TL;DR: The cell type responsible for inhibition by antigen of migration in vitro of peritoneal exudate cells obtained from tuberculin-hypersensitive guinea pigs was studied and elaborated into the medium a soluble material capable of inhibiting migration of normal exudates.