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dc.contributor.authorStrutt, T. M.
dc.contributor.authorDhume, K.
dc.contributor.authorFinn, C. M.
dc.contributor.authorHwang, J. H.
dc.contributor.authorCastonguay, Catherine
dc.contributor.authorSwain, Susan L.
dc.contributor.authorMcKinstry, K. K.
dc.date2022-08-11T08:09:50.000
dc.date.accessioned2022-08-23T16:45:21Z
dc.date.available2022-08-23T16:45:21Z
dc.date.issued2018-05-01
dc.date.submitted2018-07-06
dc.identifier.citation<p>Mucosal Immunol. 2018 May;11(3):668-680. doi: 10.1038/mi.2017.101. Epub 2017 Nov 29. <a href="https://doi.org/10.1038/mi.2017.101">Link to article on publisher's site</a></p>
dc.identifier.issn1933-0219 (Linking)
dc.identifier.doi10.1038/mi.2017.101
dc.identifier.pmid29186108
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40666
dc.description.abstractTissue-resident memory T cells (TRM) provide optimal defense at the sites of infection, but signals regulating their development are unclear, especially for CD4 T cells. Here we identify two distinct pathways that lead to the generation of CD4 TRM in the lungs following influenza infection. The TRM are transcriptionally distinct from conventional memory CD4 T cells and share a gene signature with CD8 TRM. The CD4 TRM are superior cytokine producers compared with conventional memory cells, can protect otherwise naive mice against a lethal influenza challenge, and display functional specialization by inducing enhanced inflammatory responses from dendritic cells compared with conventional memory cells. Finally, we demonstrate than an interleukin (IL)-2-dependent and a novel IL-2-independent but IL-15-dependent pathway support the generation of cohorts of lung TRM.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29186108&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5975122/
dc.subjectImmunology of Infectious Disease
dc.subjectImmunopathology
dc.subjectPathological Conditions, Signs and Symptoms
dc.subjectRespiratory Tract Diseases
dc.subjectVirus Diseases
dc.titleIL-15 supports the generation of protective lung-resident memory CD4 T cells
dc.typeJournal Article
dc.source.journaltitleMucosal immunology
dc.source.volume11
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3468
dc.identifier.contextkey12450239
html.description.abstract<p>Tissue-resident memory T cells (TRM) provide optimal defense at the sites of infection, but signals regulating their development are unclear, especially for CD4 T cells. Here we identify two distinct pathways that lead to the generation of CD4 TRM in the lungs following influenza infection. The TRM are transcriptionally distinct from conventional memory CD4 T cells and share a gene signature with CD8 TRM. The CD4 TRM are superior cytokine producers compared with conventional memory cells, can protect otherwise naive mice against a lethal influenza challenge, and display functional specialization by inducing enhanced inflammatory responses from dendritic cells compared with conventional memory cells. Finally, we demonstrate than an interleukin (IL)-2-dependent and a novel IL-2-independent but IL-15-dependent pathway support the generation of cohorts of lung TRM.</p>
dc.identifier.submissionpathoapubs/3468
dc.contributor.departmentDepartment of Pathology
dc.source.pages668-680


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