TABLE 1.
Clone (original designation)a | TCRBVb | CDR3 | TCRBJc | % Specific lysisd |
---|---|---|---|---|
EC1 (S-C003) | 25.1 | CASSEADFEAF | 1.1 | 74 |
EC2 (S-T001) | 18 | CASSPGQFSHEQY | 2.7 | 77 |
EC3 (B3) | 4.3 | CASRPGLASNEQF | 2.1 | 75 |
EC4 (B5) | 6.5 | CASRPGQGATEAF | 1.1 | 78 |
IC1 (S-C007) | 20.1 | CSARDGGEQY | 2.7 | 30 |
IC2 (B6) | 20.1 | CSARDRGTREVADNYGYT | 1.2 | 22 |
IC3 (002) | 5.6 | CASGGGTVYEQY | 2.7 | 26 |
IC4 (013) | 2 | CASSAGPGQYGNTIY | 1.3 | 16 |
IC5 (S-T002) | 7.9 | CASSLDRLEQF | 1.1 | ND |
The original designations are from reference 1.
TCRBV, TCR β-chain variable region.
TCRBJ, TCR β-chain joining (J) region.
The ability of KK10-specific effective CD8+ T-cell clones (EC) and ineffective CD8+ T-cell clones (IC) to kill GXR cells infected with NL4-3 wild-type virus was tested in the standard 4-h chromium release assay, and percent specific lysis was calculated as described in Materials and Methods. CD8+ T-cell clones EC1, EC2, IC1, and IC5 were obtained from elite controller CTR203, CD8+ T-cell clones EC3, EC4, and IC2 were obtained from elite controller FW56, and CD8+ T-cell clones IC3 and IC4 were obtained from chronic progressor CR540 (1). The ineffective functional phenotype of IC5 (as S-T002) has previously been established and reported (1). ND, not done.