Blockade of Tim-1 and Tim-4 Enhances Atherosclerosis in Low-Density Lipoprotein Receptor–Deficient Mice
Author(s) -
Amanda C. Foks,
Daniel Engelbertsen,
Felicia Kuperwaser,
Noah AlbertsGrill,
Ayelet Gonen,
Joseph L. Witztum,
James A. Lederer,
Petr Jarolı́m,
Rosemarie H. DeKruyff,
Gordon J. Freeman,
Andrew H. Lichtman
Publication year - 2016
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.115.306860
Subject(s) - efferocytosis , phosphatidylserine , immune system , apoptosis , antibody , phagocytosis , biology , t cell , blockade , microbiology and biotechnology , immunology , receptor , cancer research , chemistry , macrophage , in vitro , biochemistry , phospholipid , membrane
T cell immunoglobulin and mucin domain (Tim) proteins are expressed by numerous immune cells, recognize phosphatidylserine on apoptotic cells, and function as costimulators or coinhibitors. Tim-1 is expressed by activated T cells but is also found on dendritic cells and B cells. Tim-4, present on macrophages and dendritic cells, plays a critical role in apoptotic cell clearance, regulates the number of phosphatidylserine-expressing activated T cells, and is genetically associated with low low-density lipoprotein and triglyceride levels. Because these functions of Tim-1 and Tim-4 could affect atherosclerosis, their modulation has potential therapeutic value in cardiovascular disease.
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