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CD4(+) and CD8(+) TCR? repertoires possess different potentials to generate extraordinarily high-avidity T cells.


ABSTRACT: Recent high throughput sequencing analysis has revealed that the TCR? repertoire is largely different between CD8(+) and CD4(+) T cells. Here, we show that the transduction of SIG35?, the public chain-centric HLA-A*02:01(A2)/MART127-35 TCR? hemichain, conferred A2/MART127-35 reactivity to a substantial subset of both CD8(+) and CD4(+) T cells regardless of their HLA-A2 positivity. T cells individually reconstituted with SIG35? and different A2/MART127-35 TCR? genes isolated from CD4(+) or CD8(+) T cells exhibited a wide range of avidity. Surprisingly, approximately half of the A2/MART127-35 TCRs derived from CD4(+) T cells, but none from CD8(+) T cells, were stained by A2/MART127-35 monomer and possessed broader cross-reactivity. Our results suggest that the differences in the primary structure of peripheral CD4(+) and CD8(+) TCR? repertoire indeed result in the differences in their ability to form extraordinarily high avidity T cells which would otherwise have been deleted by central tolerance.

SUBMITTER: Nakatsugawa M 

PROVIDER: S-EPMC4814874 | biostudies-other | 2016 Mar

REPOSITORIES: biostudies-other

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CD4(+) and CD8(+) TCRβ repertoires possess different potentials to generate extraordinarily high-avidity T cells.

Nakatsugawa Munehide M   Rahman Muhammed A MA   Yamashita Yuki Y   Ochi Toshiki T   Wnuk Piotr P   Tanaka Shinya S   Chamoto Kenji K   Kagoya Yuki Y   Saso Kayoko K   Guo Tingxi T   Anczurowski Mark M   Butler Marcus O MO   Hirano Naoto N  

Scientific reports 20160331


Recent high throughput sequencing analysis has revealed that the TCRβ repertoire is largely different between CD8(+) and CD4(+) T cells. Here, we show that the transduction of SIG35α, the public chain-centric HLA-A*02:01(A2)/MART127-35 TCRα hemichain, conferred A2/MART127-35 reactivity to a substantial subset of both CD8(+) and CD4(+) T cells regardless of their HLA-A2 positivity. T cells individually reconstituted with SIG35α and different A2/MART127-35 TCRβ genes isolated from CD4(+) or CD8(+)  ...[more]

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