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dc.contributor.authorWang, Yetao
dc.contributor.authorLifshitz, Lawrence M.
dc.contributor.authorMcCauley, Sean M.
dc.contributor.authorVangala, Pranitha
dc.contributor.authorKim, Kyusik
dc.contributor.authorDerr, Alan G.
dc.contributor.authorJaiswal, Smita
dc.contributor.authorKucukural, Alper
dc.contributor.authorMcDonel, Patrick
dc.contributor.authorGreenough, Thomas C.
dc.contributor.authorHoughton, JeanMarie
dc.contributor.authorGarber, Manuel
dc.contributor.authorLuban, Jeremy
dc.date2022-08-11T08:07:59.000
dc.date.accessioned2022-08-23T15:38:08Z
dc.date.available2022-08-23T15:38:08Z
dc.date.issued2020-03-01
dc.date.submitted2020-03-18
dc.identifier.citation<p>Wang Y, Lifshitz L, Gellatly K, Vinton CL, Busman-Sahay K, McCauley S, Vangala P, Kim K, Derr A, Jaiswal S, Kucukural A, McDonel P, Hunt PW, Greenough T, Houghton J, Somsouk M, Estes JD, Brenchley JM, Garber M, Deeks SG, Luban J. HIV-1-induced cytokines deplete homeostatic innate lymphoid cells and expand TCF7-dependent memory NK cells. Nat Immunol. 2020 Mar;21(3):274-286. doi: 10.1038/s41590-020-0593-9. Epub 2020 Feb 17. PMID: 32066947; PMCID: PMC7044076. <a href="https://doi.org/10.1038/s41590-020-0593-9">Link to article on publisher's site</a></p>
dc.identifier.issn1529-2908 (Linking)
dc.identifier.doi10.1038/s41590-020-0593-9
dc.identifier.pmid32066947
dc.identifier.urihttp://hdl.handle.net/20.500.14038/25874
dc.description<p>Full author list omitted for brevity. For the full list of authors, see article.</p>
dc.description.abstractHuman immunodeficiency virus 1 (HIV-1) infection is associated with heightened inflammation and excess risk of cardiovascular disease, cancer and other complications. These pathologies persist despite antiretroviral therapy. In two independent cohorts, we found that innate lymphoid cells (ILCs) were depleted in the blood and gut of people with HIV-1, even with effective antiretroviral therapy. ILC depletion was associated with neutrophil infiltration of the gut lamina propria, type 1 interferon activation, increased microbial translocation and natural killer (NK) cell skewing towards an inflammatory state, with chromatin structure and phenotype typical of WNT transcription factor TCF7-dependent memory T cells. Cytokines that are elevated during acute HIV-1 infection reproduced the ILC and NK cell abnormalities ex vivo. These results show that inflammatory cytokines associated with HIV-1 infection irreversibly disrupt ILCs. This results in loss of gut epithelial integrity, microbial translocation and memory NK cells with heightened inflammatory potential, and explains the chronic inflammation in people with HIV-1.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=32066947&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1038/s41590-020-0593-9
dc.subjectImmunology
dc.subjectInfectious diseases
dc.subjectMicrobiology
dc.subjectMolecular biology
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectBiochemistry, Biophysics, and Structural Biology
dc.subjectBioinformatics
dc.subjectGenetics and Genomics
dc.subjectImmunology and Infectious Disease
dc.subjectMicrobiology
dc.subjectViruses
dc.subjectUMCCTS funding
dc.titleHIV-1-induced cytokines deplete homeostatic innate lymphoid cells and expand TCF7-dependent memory NK cells
dc.typeJournal Article
dc.source.journaltitleNature immunology
dc.source.volume21
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/bioinformatics_pubs/167
dc.identifier.contextkey16900473
html.description.abstract<p>Human immunodeficiency virus 1 (HIV-1) infection is associated with heightened inflammation and excess risk of cardiovascular disease, cancer and other complications. These pathologies persist despite antiretroviral therapy. In two independent cohorts, we found that innate lymphoid cells (ILCs) were depleted in the blood and gut of people with HIV-1, even with effective antiretroviral therapy. ILC depletion was associated with neutrophil infiltration of the gut lamina propria, type 1 interferon activation, increased microbial translocation and natural killer (NK) cell skewing towards an inflammatory state, with chromatin structure and phenotype typical of WNT transcription factor TCF7-dependent memory T cells. Cytokines that are elevated during acute HIV-1 infection reproduced the ILC and NK cell abnormalities ex vivo. These results show that inflammatory cytokines associated with HIV-1 infection irreversibly disrupt ILCs. This results in loss of gut epithelial integrity, microbial translocation and memory NK cells with heightened inflammatory potential, and explains the chronic inflammation in people with HIV-1.</p>
dc.identifier.submissionpathbioinformatics_pubs/167
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentGarber Lab
dc.contributor.departmentDepartment of Biochemistry and Molecular Pharmacology
dc.contributor.departmentDepartment of Medicine
dc.contributor.departmentProgram in Bioinformatics and Integrative Biology
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages274-286


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