Table 2.

Effects of the MR1 E76Q E149Q salt bridge mutations on the binding affinities of AF-7 TCR, E8 TCR, and E8 TRBV6-1 TCR

MR1 WtMR1 E76Q E149Q
TCR5-OP-RU6-FP5-FSA5-OP-RU6-FP5-FSA
AF-7 1 ± 0.02 μM >150 μM >150 μM 0.6 ± 0.03 μM >150 μM >150 μM 
E8 1.3 ± 0.1 nM 0.6 ± 0.07 μM 0.2 ± 0.03 μM 11.2 ± 1.5 nM 3.5 ± 0.2 μM 1.8 ± 0.2 μM 
E8 TRBV6-1 80.3 ± 8.3 nM 10.8 ± 0.7 μM 6.9 ± 0.9 μM 0.6 ± 0.05 μM 42.1 ± 2.6 μM 32.1 ± 3.7 μM 
MR1 WtMR1 E76Q E149Q
TCR5-OP-RU6-FP5-FSA5-OP-RU6-FP5-FSA
AF-7 1 ± 0.02 μM >150 μM >150 μM 0.6 ± 0.03 μM >150 μM >150 μM 
E8 1.3 ± 0.1 nM 0.6 ± 0.07 μM 0.2 ± 0.03 μM 11.2 ± 1.5 nM 3.5 ± 0.2 μM 1.8 ± 0.2 μM 
E8 TRBV6-1 80.3 ± 8.3 nM 10.8 ± 0.7 μM 6.9 ± 0.9 μM 0.6 ± 0.05 μM 42.1 ± 2.6 μM 32.1 ± 3.7 μM 

Binding affinities, as measured by surface plasmon resonance, of the AF-7, E8 TCR, and E8 TRBV6-1 TCR interacting with wildtype MR1 and MR1 E76Q E149Q refolded with 5-OP-RU, 6-FP, and 5-FSA. >150 μM: the measured KD of the TCR MR1 interaction was >150 μM and therefore is unlikely to generate a MAIT cell response. KD are indicated with the standard error in brackets. The binding affinity of the E8 TCR to MR1 5-OP-RU and MR1 E76Q E149Q 5-OP-RU was measured using the BIAcore8K using single-cycle kinetic analysis. The remining measurements were completed on a BiacoreT200 and the KDs were calculated using steady-state analysis.

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