William A. Boisvert
University of Hawaii at Manoa
91 Papers
427 Citations
William A. Boisvert is an academic researcher from University of Hawaii at Manoa. The author has contributed to research in topics: Inflammation & Macrophage. The author has an hindex of 36, co-authored 91 publications. Previous affiliations of William A. Boisvert include University of Oregon & Tufts University.
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Papers
A leukocyte homologue of the IL-8 receptor CXCR-2 mediates the accumulation of macrophages in atherosclerotic lesions of LDL receptor-deficient mice.
TL;DR: The capacity of leukocytes to express mIL-8RH, and associated intralesional expression of its ligands such as KC/GROalpha, mediated the intimal accumulation of macrophages in atherosclerotic lesions of LDL receptor-deficient mice.
Inflammation in Atherosclerosis. Lesion Formation in LDL Receptor--Deficient Mice With Perforin and Lyst beige Mutations
TL;DR: The Lystbeige mutation in LDLr−/− mice has proatherogenic properties that are independent of NK cell–mediated cytolysis and lymphocyte-mediated acquired immunity.
433
Overexpression of Interleukin-10 by Activated T Lymphocytes Inhibits Atherosclerosis in LDL Receptor–Deficient Mice by Altering Lymphocyte and Macrophage Phenotypes
Laura J. Pinderski,Michael P. Fischbein,Ganesamoorthy Subbanagounder,Michael C. Fishbein,Nobuhiko Kubo,Hilde Cheroutre,Linda K. Curtiss,Judith A. Berliner,William A. Boisvert +8 more
TL;DR: It is demonstrated that T lymphocyte IL-10 can influence the function of other immune cells to reduce the development of advanced atherosclerotic lesions in mice.
379
Role of tissue factor and protease-activated receptors in a mouse model of endotoxemia
Rafal Pawlinski,Brian Pedersen,Gernot Schabbauer,Michael Tencati,Todd Holscher,William A. Boisvert,Patricia Andrade-Gordon,Rolf Dario Frank,Nigel Mackman +8 more
TL;DR: Data demonstrate that hematopoietic cells are the major pathologic site of TF expression during endotoxemia and suggest that multiple protease-activated receptors mediate crosstalk between coagulation and inflammation.
314
Apolipoprotein E and atherosclerosis.
TL;DR: The lesion apolipoprotein E directly modifies both macrophage- and T lymphocyte-mediated immune responses that contribute to this chronic inflammatory disease.
280