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Evidence that macrophages are programmed to die after activating autologous, cloned, antigen-specific, CD4 + T cells

dc.contributor.authorRichardson, Bruce C.en_US
dc.contributor.authorBuckmaster, Tareken_US
dc.contributor.authorKeren, David F.en_US
dc.contributor.authorJohnson, Kent J.en_US
dc.date.accessioned2006-04-28T16:33:15Z
dc.date.available2006-04-28T16:33:15Z
dc.date.issued1993-07en_US
dc.identifier.citationRichardson, Bruce C.; Buckmaster, Tarek; Keren, David F.; Johnson, Kent J. (1993)."Evidence that macrophages are programmed to die after activating autologous, cloned, antigen-specific, CD4 + T cells." European Journal of Immunology 23(7): 1450-1455. <http://hdl.handle.net/2027.42/37962>en_US
dc.identifier.issn0014-2980en_US
dc.identifier.issn1521-4141en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/37962
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8100771&dopt=citationen_US
dc.description.abstractThe bone marrow produces large numbers of monocytes daily, but the mechanisms balancing production and elimination are unknown. In this report we demonstrate that macrophages (Mφ) undergo apoptosis after activating autologous CD4 + cells. Since apoptosis is a genetically programmed response, these results argue that MΦ death can be part of a normal immune response. This event may have relevance to monocyte/Mφ homeostasis, as well as immune response regulation and host defenses to intracellular organisms.en_US
dc.format.extent933596 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherWILEY-VCH Verlag GmbHen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherMicrobiology and Immunologyen_US
dc.titleEvidence that macrophages are programmed to die after activating autologous, cloned, antigen-specific, CD4 + T cellsen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelBiological Chemistryen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Pathology, University of Michigan, Ann Arbor, Kalamazoo ; Bruce Richardson, R4540 Kresge 1, Ann Arbor, MI 48109-0531, USAen_US
dc.contributor.affiliationumDepartment of Medicine, University of Michigan, Ann Arbor, Kalamazooen_US
dc.contributor.affiliationumDepartment of Medicine, University of Michigan, Ann Arbor, Kalamazooen_US
dc.contributor.affiliationotherAnn Arbor Veterans Administration Hospital, Ann Arbor and Kalamazoo College, Kalamazooen_US
dc.identifier.pmid8100771en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/37962/1/1830230708_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/(ISSN)1521-4141en_US
dc.identifier.sourceEuropean Journal of Immunologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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