| Role of target and effector cell structures in natural killer-mediated cytotoxicity. | |
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MedLine Citation:
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PMID: 3809889 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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An analysis of target and effector cell structures involved in the in vitro natural killer (NK)-mediated cytotoxicity has been performed. The degree of surface expression of transferrin receptor (TR) was only in part correlated with that of cell lysis. Moreover, the lysis could not be blocked by treating target cells with two anti-TR monoclonal antibodies. Finally, cell lines poorly affected by NK cells express TR only at the cytoplasmic level. As to the effector cells, the integrity of cytoskeleton components (especially microtubules) was found to be essential for the occurrence of cell lysis. In fact, vinblastine, an anti-microtubule agent, was able to significantly reduce the percentage cell lysis. This effect was not due to a selective depletion in NK cells induced by the drug. It is concluded that the mechanisms underlying NK activity are complex and involve both target and effector cell structures. |
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Authors:
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P L Tazzari; D Zauli; D Raspadori; C Crespi; M Magnani; A Tassinari; M Gobbi |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: La Ricerca in clinica e in laboratorio Volume: 16 ISSN: 0390-5748 ISO Abbreviation: Ric Clin Lab Publication Date: 1986 Jul-Sep |
Date Detail:
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Created Date: 1987-03-17 Completed Date: 1987-03-17 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7613947 Medline TA: Ric Clin Lab Country: ITALY |
Other Details:
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Languages: eng Pagination: 443-7 Citation Subset: IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Cell Line Cytoskeleton / physiology* Cytotoxicity, Immunologic* Humans Killer Cells, Natural / immunology* Microtubules / physiology Receptors, Transferrin / analysis* Vinblastine / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Receptors, Transferrin; 865-21-4/Vinblastine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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