Please use this identifier to cite or link to this item:
Title: Non-canonicaly recruited TCRαβCD8αα IELs recognize microbial antigens
Authors: Wojciech, L. 
Szurek, E.
Kuczma, M.
Cebula, A.
Elhefnawy, W.R.
Pietrzak, M.
Rempala, G.
Ignatowicz, L.
Issue Date: 2018
Publisher: Nature Publishing Group
Citation: Wojciech, 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.
Rights: Attribution 4.0 International
Abstract: In 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).
Source Title: Scientific Reports
ISSN: 2045-2322
DOI: 10.1038/s41598-018-29073-7
Rights: Attribution 4.0 International
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1038_s41598-018-29073-7.pdf4.1 MBAdobe PDF



Google ScholarTM



This item is licensed under a Creative Commons License Creative Commons