H
Henry B. Warren
Researcher at Harvard University
Publications - 22
Citations - 2987
Henry B. Warren is an academic researcher from Harvard University. The author has contributed to research in topics: Inflammation & Antibody. The author has an hindex of 18, co-authored 22 publications receiving 2889 citations. Previous affiliations of Henry B. Warren include Brigham and Women's Hospital.
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Journal ArticleDOI
A mouse model of human familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism
Chrystal Ho,David A. Conner,Martin R. Pollak,Martin R. Pollak,Daniel Ladd,Daniel Ladd,Olga Kifor,Henry B. Warren,Edward M. Brown,Jonathan G. Seidman,Christine E. Seidman +10 more
TL;DR: The findings suggest that Casr mutations cause these human disorders by reducing the number of functional receptor molecules on the cell surface.
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Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity
TL;DR: Results indicate that the alternative pathway is sufficient to mediate effective opsonophagocytosis and protective immunity to GBS in the presence of specific antibody, and implies that the classical pathway plays an essential role in host defense against GBS infection in the absence of specific immunity.
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Tsc2+/– mice develop tumors in multiple sites that express gelsolin and are influenced by genetic background
TL;DR: In this article, the authors developed a murine model of TSC2 disease using a gene targeting approach and found that Tsc2-null embryos die at embryonic days 9.5-12.5 from hepatic hypoplasia.
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Immunoglobulin G–mediated Inflammatory Responses Develop Normally in Complement-deficient Mice
Diana Sylvestre,Raphael Clynes,Minga Ma,Henry B. Warren,Michael C. Carroll,Jeffrey V. Ravetch +5 more
TL;DR: These studies provide strong evidence that the activation of cell-based FcγR receptors, but not complement, are required for antibody-triggered murine inflammatory responses.
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Molecular analysis of the role of the group A streptococcal cysteine protease, hyaluronic acid capsule, and M protein in a murine model of human invasive soft-tissue infection.
TL;DR: It is concluded that the group A streptococcal hyaluronic acid capsule and M protein, but not the cysteine protease, are critical for the development of tissue necrosis, secondary bacteremia, and lethal infection in a murine model of human necrotizing fasciitis.