{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["6"],"submitter":["Santiago-Cruz W"],"pubmed_abstract":["CD38 is a transmembrane glycoprotein involved in NAD<sup>+</sup> metabolism, calcium signaling, and immune cell activation. Its role in the inflammatory response has been studied extensively in innate immune cells; however, its contribution to the activation of memory T lymphocytes under inflammatory conditions is less understood. Additionally, recent studies have shown an age-related increase in the expression of the protein CD38 in various human and murine tissues. Moreover, CD8<sup>+</sup> bystander T cells have been shown to contribute to inflammation during the aging process. Given the importance of its potential role in age-related pathologies, we examined the effect of CD38 on bystander activation of CD8<sup>+</sup> memory T cells in aged mice following lipopolysaccharide challenge. CD38-deficient mice exhibited attenuated serum cytokine responses (IL-1β, IL-6, IFN-γ, and IL-10) and a distinct CD8<sup>+</sup> T cell profile, characterized by a decrease in activated T cells. Wild-type mice displayed a significant expansion of CD69<sup>+</sup>T<sub>CM</sub> cells after LPS inoculation, an effect that was absent in CD38-deficient animals. LPS also promoted the expression of CD69 and CD38 in T<sub>EM/EFF</sub> subsets. Thus, our findings reveal a CD38-dependent mechanism underlying bystander activation of memory CD8<sup>+</sup> T cells in aging. Highlighting the potential contribution of CD38 to age-related diseases, such as autoimmunity, and in the face of inflammatory conditions in aged people."],"journal":["Frontiers in aging"],"pagination":["1701685"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12757697"],"repository":["biostudies-literature"],"pubmed_title":["CD38 promotes LPS-induced innate-like activation and proliferation of CD8&lt;sup&gt;+&lt;/sup&gt; T lymphocytes in aged mice."],"pmcid":["PMC12757697"],"pubmed_authors":["Perez-Lara JC","Garcia-Garcia F","Rodriguez-Alba JC","Espinosa E","Devarajan P","Santiago-Cruz W","Romero-Ramirez H"],"additional_accession":[]},"is_claimable":false,"name":"CD38 promotes LPS-induced innate-like activation and proliferation of CD8&lt;sup&gt;+&lt;/sup&gt; T lymphocytes in aged mice.","description":"CD38 is a transmembrane glycoprotein involved in NAD<sup>+</sup> metabolism, calcium signaling, and immune cell activation. Its role in the inflammatory response has been studied extensively in innate immune cells; however, its contribution to the activation of memory T lymphocytes under inflammatory conditions is less understood. Additionally, recent studies have shown an age-related increase in the expression of the protein CD38 in various human and murine tissues. Moreover, CD8<sup>+</sup> bystander T cells have been shown to contribute to inflammation during the aging process. Given the importance of its potential role in age-related pathologies, we examined the effect of CD38 on bystander activation of CD8<sup>+</sup> memory T cells in aged mice following lipopolysaccharide challenge. CD38-deficient mice exhibited attenuated serum cytokine responses (IL-1β, IL-6, IFN-γ, and IL-10) and a distinct CD8<sup>+</sup> T cell profile, characterized by a decrease in activated T cells. Wild-type mice displayed a significant expansion of CD69<sup>+</sup>T<sub>CM</sub> cells after LPS inoculation, an effect that was absent in CD38-deficient animals. LPS also promoted the expression of CD69 and CD38 in T<sub>EM/EFF</sub> subsets. Thus, our findings reveal a CD38-dependent mechanism underlying bystander activation of memory CD8<sup>+</sup> T cells in aging. Highlighting the potential contribution of CD38 to age-related diseases, such as autoimmunity, and in the face of inflammatory conditions in aged people.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-06-06T10:37:58.829Z","creation":"2026-05-29T03:12:08.391Z"},"accession":"S-EPMC12757697","cross_references":{"pubmed":["41488275"],"doi":["10.3389/fragi.2025.1701685"]}}