Long-term rapamycin treatment suppresses IL-17-producing gamma delta T cells and blunts neuroinflammation in aging

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dc.contributor.authorTorrent, Clement
dc.contributor.authorGagliardi, Caterina
dc.contributor.authorFülle, Nina
dc.contributor.authorAntignano, Ignazio
dc.contributor.authorBernis, Maria Eugenia
dc.contributor.authorStork, Miriam
dc.contributor.authorBano, Daniele
dc.contributor.authorCapasso, Melania
dc.contributor.authorKeane, Lily
dc.contributor.funderCancer Research UK Cambridge Institute
dc.contributor.funderAge UK
dc.date.accessioned2026-08-19T11:51:01Z
dc.date.available2026-08-19T11:51:01Z
dc.date.issued2026-05-28
dc.description© 2026, Torrent et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.description.abstractAging is the gradual accumulation of structural and functional changes in an organism over time, including immune remodeling and a progressive increase in basal inflammation, or inflammaging. The mTOR pathway is a central driver of aging-related diseases, such as cancer, chronic inflammation and neurodegeneration; pharmacological inhibition with rapamycin is associated with reduced aged-related morbidity and increased lifespan across species. Nonetheless, concerns remain about the use of rapamycin, a well-established immunosuppressant in transplant medicine, as an anti-aging intervention. Here, we evaluated the impact of prolonged low-dose dietary rapamycin on the aging immune system. Treatment did not significantly alter innate or adaptive immune cell populations, including brain resident microglia; however, it attenuated the age-associated accumulation of IL-17–producing γδ T cells, particularly in the peritoneal cavity. After a peripheral inflammatory LPS challenge, circulating IL-17 levels were significantly reduced and correlated with an attenuation of microglia inflammatory phenotype. These findings suggest that prolonged low-dose rapamycin exposure exerts minor systemic immune changes, while selectively limiting age-related γδ T cell expansion and neuroinflammation associated with systemic inflammation.en
dc.description.sponsorshipCancer Research UK|C16420/A18066
dc.format.extent17
dc.format.extent1626203
dc.identifier.articleide0343183
dc.identifier.authororcidTorrent, Clement
dc.identifier.authororcidGagliardi, Caterina
dc.identifier.authororcidFülle, Nina
dc.identifier.authororcidAntignano, Ignazio
dc.identifier.authororcidBernis, Maria Eugenia
dc.identifier.authororcidStork, Miriam
dc.identifier.authororcidBano, Daniele
dc.identifier.authororcidCapasso, Melania
dc.identifier.authororcidKeane, Lily§0000-0001-7418-3434
dc.identifier.citationTorrent, C, Gagliardi, C, Fülle, N, Antignano, I, Bernis, M E, Stork, M, Bano, D, Capasso, M & Keane, L 2026, 'Long-term rapamycin treatment suppresses IL-17-producing gamma delta T cells and blunts neuroinflammation in aging', PLOS ONE, vol. 21, no. 5, e0343183, pp. 1-17. https://doi.org/10.1371/journal.pone.0343183
dc.identifier.doi10.1371/journal.pone.0343183
dc.identifier.endpage17
dc.identifier.issn1932-6203
dc.identifier.issued5
dc.identifier.journaltitlePLOS ONE
dc.identifier.otherORCID: /0000-0001-7418-3434/work/224336012
dc.identifier.startpage1
dc.identifier.urihttps://hdl.handle.net/10468/19129
dc.identifier.urlhttps://www.scopus.com/pages/publications/105040054969
dc.identifier.volume21
dc.language.isoeng
dc.rightscc_by
dc.subjectSDG 3 - Good Health and Well-being
dc.subjectLong-term rapamycin treatment
dc.subjectmTOR pathway
dc.subjectLow-dose dietary rapamycin
dc.subjectNeuroinflammation
dc.subject[Medicine]
dc.subject[APCMicrobiome]
dc.subjectMultidisciplinary
dc.titleLong-term rapamycin treatment suppresses IL-17-producing gamma delta T cells and blunts neuroinflammation in agingen
dc.typeArticle (Peer reviewed)
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