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Dissecting the IFN-g versus IL-17-specific mRNAomes of effector gd T lymphocytes

2022-11Conference object Open access
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dc.contributor.authorInácio, Daniel
dc.contributor.authorPamplona, Ana
dc.contributor.authorAmado, Tiago
dc.contributor.authorSobral, Daniel
dc.contributor.authorCunha, Carolina
dc.contributor.authorGomes, Anita Q.
dc.contributor.authorSilva-Santos, Bruno
dc.date.accessioned2024-01-16T13:07:18Z
dc.date.available2024-01-16T13:07:18Z
dc.date.issued2022-11
dc.description.abstractThe ability of murine γδ T cells to rapidly produce the pro-inflammatory cytokines interleukin-17 (IL-17) or interferon-γ (IFN-γ) underlies their crucial roles in several pathophysiological contexts, from infection to cancer or autoimmunity. This functional capacity stems from a complex process of ‘developmental pre-programming’ in the thymus, after which a significant fraction of γδ T cells migrate to peripheral sites already committed to producing either IL-17 (gd17) or IFN-γ (gdIFN). While several studies have studied these gd T cell subtypes using surface markers that enrich for effector function, we still lack a characterization of the mRNA transcriptomes that specifically associate with IL-17 or IFN-g production by gd T cells. To overcome this limitation, in this study, we established a double reporter IL-17-GFP:IFN-γ-YFP mouse strain, which allowed us to isolate pure IL-17+, IFN-γ+, and the remaining IL-17-IFN-g-(DN) γδ T cell populations from the peripheral lymphoid organs to perform RNA sequencing and identify the subset-specific mRNAomes. Overall, we detected the expression of 12822 genes in gd T cells, with a significant number of genes being enriched in gd17 when compared with gdIFN and gdDN cells. Among these, 936 genes were differentially expressed between the three populations, with gd17 and gdIFN cells displaying the most distinct mRNAomes, which highlights their functional specialization, and gdIFN being more similar to DN than gd17 cells. A more detailed analysis of the top 30 differentially expressed genes among the most expressed genes by gd17 and gdIFN cells revealed that the majority of the signature genes increase their expression levels in the periphery upon their egress from the thymus, suggesting that these effector subsets only terminate their differentiation process at peripheral sites. Notably, gd17-associated signature genes are specifically expressed in this subset, unlike gdIFN signature genes, which are also often expressed by gdDN T cells, thus suggesting a developmental relationship between these two subpopulations. Collectively, our data allowed us to identify distinct mRNA signatures directly associated with cytokine expression in γδ T cells, several of which we are now further studying in disease models to identify potential new roles in pathophysiology.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationInácio D, Pamplona A, Amado T, Sobral D, Cunha C, Gomes AQ, et al. Dissecting the IFN-g versus IL-17-specific mRNAomes of effector gd T lymphocytes. In: Gene Expression and Signaling in the Immune System, Cold Spring Harbor Laboratory (CSHL) [virtual meeting], November 1-5, 2022.pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.21/16897
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relation.publisherversionhttps://meetings.cshl.edu/meetings.aspx?meet=IMMUNE&year=22pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectIFN-γpt_PT
dc.subjectIL-17-specific transcriptomespt_PT
dc.subjectγδ T lymphocytespt_PT
dc.subjectThemispt_PT
dc.titleDissecting the IFN-g versus IL-17-specific mRNAomes of effector gd T lymphocytespt_PT
dc.typeconference object
dspace.entity.typePublication
person.familyNameGomes
person.givenNameAnita
person.identifier.ciencia-id4B10-E015-52B7
person.identifier.orcid0000-0002-3348-0448
person.identifier.ridC-3580-2014
person.identifier.scopus-author-id7202386033
rcaap.rightsopenAccesspt_PT
rcaap.typeconferenceObjectpt_PT
relation.isAuthorOfPublication2b5a3f0a-29c2-4ecd-a83f-50d0b99a4875
relation.isAuthorOfPublication.latestForDiscovery2b5a3f0a-29c2-4ecd-a83f-50d0b99a4875

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