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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)/MART1 27–35  TCRα hemichain, conferred A2/MART1 27–35  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/MART1 27–35  TCRβ genes isolated from CD4 +  or CD8 +  T cells exhibited a wide range of avidity. Surprisingly, approximately half of the A2/MART1 27–35  TCRs derived from CD4 +  T cells, but none from CD8 +  T cells, were stained by A2/MART1 27–35  monomer and possessed broader cross-reactivity. Our results suggest that the differences in the primary structure of peripheral CD4 +  and CD8 +  TCRβ 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.

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