{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Novais FO"],"funding":["NIAID NIH HHS"],"pagination":["1737-1745"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6178231"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["200(5)"],"pubmed_abstract":["Resolution of leishmaniasis depends upon parasite control and limiting inflammation. CD4+ Th1 cells are required to control parasites, whereas CD8+ T cells play a dual role: they promote Th1 cell differentiation but can also increase inflammation at the site of infection as a consequence of cytolysis. Although CD8+ T cells taken from leishmanial lesions are cytolytic, in this study, we showed that only a few CD8+ T cells produced IFN-?. Correspondingly, only low levels of IL-12 and/or IL-12 mRNA were present in lesions from infected mice, as well as patients. Addition of IL-12 increased IFN-? production by CD8+ T cells isolated from leishmanial lesions, suggesting that a lack of IL-12 at the site of infection limits IFN-? production by CD8+ T cells. To determine whether CD8+ T cells could promote resistance in vivo if IL-12 was present, we administered IL-12 to Leishmania-infected RAG mice reconstituted with CD8+ T cells. IL-12 treatment increased the ability of CD8+ T cells to make IFN-?, but CD8+ T cells still failed to control the parasites. Furthermore, despite the ability of CD8+ T cells to promote immunity to secondary infections, we also found that CD8+ T cells from immune mice were unable to control Leishmania in RAG mice. Taken together, these results indicate that lesional CD8+ T cells fail to make IFN-? because of a deficit in IL-12 but that, even with IL-12, CD8+ T cells are unable to control Leishmania in the absence of CD4+ T cells."],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["CD8+ T Cells Lack Local Signals To Produce IFN-? in the Skin during Leishmania Infection."],"pmcid":["PMC6178231"],"funding_grant_id":["R01 AI106842"],"pubmed_authors":["Villareal DO","Wong AC","Scott P","Novais FO","Beiting DP"],"additional_accession":[]},"is_claimable":false,"name":"CD8+ T Cells Lack Local Signals To Produce IFN-? in the Skin during Leishmania Infection.","description":"Resolution of leishmaniasis depends upon parasite control and limiting inflammation. CD4+ Th1 cells are required to control parasites, whereas CD8+ T cells play a dual role: they promote Th1 cell differentiation but can also increase inflammation at the site of infection as a consequence of cytolysis. Although CD8+ T cells taken from leishmanial lesions are cytolytic, in this study, we showed that only a few CD8+ T cells produced IFN-?. Correspondingly, only low levels of IL-12 and/or IL-12 mRNA were present in lesions from infected mice, as well as patients. Addition of IL-12 increased IFN-? production by CD8+ T cells isolated from leishmanial lesions, suggesting that a lack of IL-12 at the site of infection limits IFN-? production by CD8+ T cells. To determine whether CD8+ T cells could promote resistance in vivo if IL-12 was present, we administered IL-12 to Leishmania-infected RAG mice reconstituted with CD8+ T cells. IL-12 treatment increased the ability of CD8+ T cells to make IFN-?, but CD8+ T cells still failed to control the parasites. Furthermore, despite the ability of CD8+ T cells to promote immunity to secondary infections, we also found that CD8+ T cells from immune mice were unable to control Leishmania in RAG mice. Taken together, these results indicate that lesional CD8+ T cells fail to make IFN-? because of a deficit in IL-12 but that, even with IL-12, CD8+ T cells are unable to control Leishmania in the absence of CD4+ T cells.","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Mar","modification":"2020-11-19T16:31:24Z","creation":"2019-06-06T20:16:55Z"},"accession":"S-EPMC6178231","cross_references":{"pubmed":["29367210"],"doi":["10.4049/jimmunol.1701597"]}}