IL-15 supports the generation of protective lung-resident memory CD4 T cells
dc.contributor.author | Strutt, T. M. | |
dc.contributor.author | Dhume, K. | |
dc.contributor.author | Finn, C. M. | |
dc.contributor.author | Hwang, J. H. | |
dc.contributor.author | Castonguay, Catherine | |
dc.contributor.author | Swain, Susan L. | |
dc.contributor.author | McKinstry, K. K. | |
dc.date | 2022-08-11T08:09:50.000 | |
dc.date.accessioned | 2022-08-23T16:45:21Z | |
dc.date.available | 2022-08-23T16:45:21Z | |
dc.date.issued | 2018-05-01 | |
dc.date.submitted | 2018-07-06 | |
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.issn | 1933-0219 (Linking) | |
dc.identifier.doi | 10.1038/mi.2017.101 | |
dc.identifier.pmid | 29186108 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/40666 | |
dc.description.abstract | 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. | |
dc.language.iso | en_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.url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5975122/ | |
dc.subject | Immunology of Infectious Disease | |
dc.subject | Immunopathology | |
dc.subject | Pathological Conditions, Signs and Symptoms | |
dc.subject | Respiratory Tract Diseases | |
dc.subject | Virus Diseases | |
dc.title | IL-15 supports the generation of protective lung-resident memory CD4 T cells | |
dc.type | Journal Article | |
dc.source.journaltitle | Mucosal immunology | |
dc.source.volume | 11 | |
dc.source.issue | 3 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/oapubs/3468 | |
dc.identifier.contextkey | 12450239 | |
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.submissionpath | oapubs/3468 | |
dc.contributor.department | Department of Pathology | |
dc.source.pages | 668-680 |