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dc.contributor.authorJangalwe, Sonal
dc.contributor.authorKapoor, Varun N.
dc.contributor.authorXu, Jia
dc.contributor.authorGirnius, Nomeda
dc.contributor.authorKennedy, Norman J.
dc.contributor.authorEdwards, Yvonne J. K.
dc.contributor.authorWelsh, Raymond M.
dc.contributor.authorDavis, Roger J.
dc.contributor.authorBrehm, Michael A.
dc.date2022-08-11T08:10:17.000
dc.date.accessioned2022-08-23T17:03:13Z
dc.date.available2022-08-23T17:03:13Z
dc.date.issued2019-02-01
dc.date.submitted2019-07-08
dc.identifier.citation<p>J Immunol. 2019 Feb 1;202(3):647-651. doi: 10.4049/jimmunol.1800278. Epub 2019 Jan 4. <a href="https://doi.org/10.4049/jimmunol.1800278">Link to article on publisher's site</a></p>
dc.identifier.issn0022-1767 (Linking)
dc.identifier.doi10.4049/jimmunol.1800278
dc.identifier.pmid30610162
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44379
dc.description.abstractApoptosis of CD8 T cells is an essential mechanism that maintains immune system homeostasis, prevents autoimmunity, and reduces immunopathology. CD8 T cell death also occurs early during the response to both inflammation and costimulation blockade (CoB). In this article, we studied the effects of a combined deficiency of Fas (extrinsic pathway) and Bim (intrinsic pathway) on early T cell attrition in response to lymphocytic choriomeningitis virus infection and during CoB during transplantation. Loss of Fas and Bim function in Bcl2l11(-/-)Fas(lpr/lpr) mice inhibited apoptosis of T cells and prevented the early T cell attrition resulting from lymphocytic choriomeningitis virus infection. Bcl2l11(-/-)Fas(lpr/lpr) mice were also resistant to prolonged allograft survival induced by CoB targeting the CD40-CD154 pathway. These results demonstrate that both extrinsic and intrinsic apoptosis pathways function concurrently to regulate T cell homeostasis during the early stages of immune responses and allograft survival during CoB.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=30610162&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.4049/jimmunol.1800278
dc.subjectHemic and Immune Systems
dc.subjectImmunology and Infectious Disease
dc.titleCutting Edge: Early Attrition of Memory T Cells during Inflammation and Costimulation Blockade Is Regulated Concurrently by Proapoptotic Proteins Fas and Bim
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume202
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pmm_pp/107
dc.identifier.contextkey14880298
html.description.abstract<p>Apoptosis of CD8 T cells is an essential mechanism that maintains immune system homeostasis, prevents autoimmunity, and reduces immunopathology. CD8 T cell death also occurs early during the response to both inflammation and costimulation blockade (CoB). In this article, we studied the effects of a combined deficiency of Fas (extrinsic pathway) and Bim (intrinsic pathway) on early T cell attrition in response to lymphocytic choriomeningitis virus infection and during CoB during transplantation. Loss of Fas and Bim function in Bcl2l11(-/-)Fas(lpr/lpr) mice inhibited apoptosis of T cells and prevented the early T cell attrition resulting from lymphocytic choriomeningitis virus infection. Bcl2l11(-/-)Fas(lpr/lpr) mice were also resistant to prolonged allograft survival induced by CoB targeting the CD40-CD154 pathway. These results demonstrate that both extrinsic and intrinsic apoptosis pathways function concurrently to regulate T cell homeostasis during the early stages of immune responses and allograft survival during CoB.</p>
dc.identifier.submissionpathpmm_pp/107
dc.contributor.departmentDavis Lab
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages647-651


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