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dc.titleNon-canonicaly recruited TCRαβCD8αα IELs recognize microbial antigens
dc.contributor.authorWojciech, L.
dc.contributor.authorSzurek, E.
dc.contributor.authorKuczma, M.
dc.contributor.authorCebula, A.
dc.contributor.authorElhefnawy, W.R.
dc.contributor.authorPietrzak, M.
dc.contributor.authorRempala, G.
dc.contributor.authorIgnatowicz, L.
dc.identifier.citationWojciech, L., Szurek, E., Kuczma, M., Cebula, A., Elhefnawy, W.R., Pietrzak, M., Rempala, G., Ignatowicz, L. (2018). Non-canonicaly recruited TCRαβCD8αα IELs recognize microbial antigens. Scientific Reports 8 (1) : 10848. ScholarBank@NUS Repository.
dc.description.abstractIn the gut, various subsets of intraepithelial T cells (IELs) respond to self or non-self-antigens derived from the body, diet, commensal and pathogenic microbiota. Dominant subset of IELs in the small intestine are TCRαβCD8αα+ cells, which are derived from immature thymocytes that express self-reactive TCRs. Although most of TCRαβCD8αα+ IELs are thymus-derived, their repertoire adapts to microbial flora. Here, using high throughput TCR sequencing we examined how clonal diversity of TCRαβCD8αα+ IELs changes upon exposure to commensal-derived antigens. We found that fraction of CD8αα+ IELs and CD4+ T cells express identical αβTCRs and this overlap raised parallel to a surge in the diversity of microbial flora. We also found that an opportunistic pathogen (Staphylococcus aureus) isolated from mouse small intestine specifically activated CD8αα+ IELs and CD4+ derived T cell hybridomas suggesting that some of TCRαβCD8αα+ clones with microbial specificities have extrathymic origin. We also report that CD8ααCD4+ IELs and Foxp3CD4+ T cells from the small intestine shared many αβTCRs, regardless whether the later subset was isolated from Foxp3CNS1 sufficient or Foxp3CNS1 deficient mice that lacks peripherally-derived Tregs. Overall, our results imply that repertoire of TCRαβCD8αα+ in small intestine expends in situ in response to changes in microbial flora. © 2018 The Author(s).
dc.publisherNature Publishing Group
dc.rightsAttribution 4.0 International
dc.sourceScopus OA2018
dc.contributor.departmentMICROBIOLOGY AND IMMUNOLOGY
dc.description.sourcetitleScientific Reports
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