Figure 6.
Different T-cell clonal signatures of maximal recall response to NLV when providing copotentiation with anti-CD3 mono-Fab. (A) Maximum recall response of private immunodominant TCR clones to exogenous NLV is mainly caused by the peptide (arrow, red segment), with a smaller contribution coming from copotentiation delivered by anti-CD3 mono-Fab (arrow, yellow segment). (B) Maximum recall immunodominant response of public TCR clones to NLV is driven by either (1) copotentiation (left arrow, yellow segment), with the smallest contribution from natural amounts of NLV presented in HCMV(+) APCs; or (2) exogenous NLV alone (right arrow). (C) NLV weak TCR clones reach their maximum recall response to exogenous NLV mainly by copotentiation (arrow, yellow segment), with a smaller contribution coming from exogenous NLV peptide (arrow, red segment). Created with BioRender.

Different T-cell clonal signatures of maximal recall response to NLV when providing copotentiation with anti-CD3 mono-Fab. (A) Maximum recall response of private immunodominant TCR clones to exogenous NLV is mainly caused by the peptide (arrow, red segment), with a smaller contribution coming from copotentiation delivered by anti-CD3 mono-Fab (arrow, yellow segment). (B) Maximum recall immunodominant response of public TCR clones to NLV is driven by either (1) copotentiation (left arrow, yellow segment), with the smallest contribution from natural amounts of NLV presented in HCMV(+) APCs; or (2) exogenous NLV alone (right arrow). (C) NLV weak TCR clones reach their maximum recall response to exogenous NLV mainly by copotentiation (arrow, yellow segment), with a smaller contribution coming from exogenous NLV peptide (arrow, red segment). Created with BioRender.

Close Modal

or Create an Account

Close Modal
Close Modal