| CD45-mediated fodrin cleavage during galectin-1 T cell death promotes phagocytic clearance of dying cells. | |
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MedLine Citation:
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PMID: 19454697 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Disassembly and phagocytic removal of dying cells is critical to maintain immune homeostasis. The factors that regulate fragmentation and uptake of dying lymphocytes are not well understood. Degradation of fodrin, a cytoskeletal linker molecule that attaches CD45 to the actin cytoskeleton, has been described in apoptotic cells, although no specific initiator of fodrin degradation has been identified. CD45 is a glycoprotein receptor for galectin-1, an endogenous lectin that can trigger lymphocyte apoptosis, although CD45 is not required for phosphatidylserine externalization or DNA degradation during galectin-1 death. In this study, we show that fodrin degradation occurs during galectin-1 T cell death and that CD45 is essential for fodrin degradation to occur. In the absence of CD45, or if fodrin degradation is prevented, galectin-1-induced cell death is not accompanied by membrane blebbing, although phosphatidylserine externalization and DNA degradation proceed, indicating that fodrin degradation occurs via a distinct pathway compared with the pathway that leads to these other hallmarks of cell death. Moreover, there is slower phagocytic uptake by macrophages of T cells in which fodrin degradation is prevented, relative to T cells in which CD45-mediated fodrin degradation occurs. These studies identify a novel role for CD45 in regulating cellular disassembly and promoting phagocytic clearance during galectin-1-induced T cell death. |
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Authors:
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Mabel Pang; Jiale He; Pauline Johnson; Linda G Baum |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 182 ISSN: 1550-6606 ISO Abbreviation: J. Immunol. Publication Date: 2009 Jun |
Date Detail:
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Created Date: 2009-05-20 Completed Date: 2009-06-22 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 7001-8 Citation Subset: AIM; IM |
Affiliation:
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Department of Pathology and Laboratory Medicine, University of California Los Angeles School of Medicine, Los Angeles, CA 90095, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Antigens, CD45
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metabolism* Apoptosis / immunology* Carrier Proteins / metabolism* Galectin 1 / physiology* Homeostasis / immunology Humans Jurkat Cells Macrophages / immunology Microfilament Proteins / metabolism* Phagocytosis* T-Lymphocytes / cytology* |
| Grant Support | |
ID/Acronym/Agency:
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AI28697/AI/NIAID NIH HHS; CA16042/CA/NCI NIH HHS; R01GM63281/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Carrier Proteins; 0/Galectin 1; 0/Microfilament Proteins; 0/fodrin; EC 3.1.3.48/Antigens, CD45 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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