Journal
CELL REPORTS
Volume 26, Issue 12, Pages 3369-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2019.02.074
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Funding
- Wellcome Trust [212343/Z/18/Z]
- EPSRC [EP/S004459/1]
- Micron, an Oxford-wide advanced microscopy technology consortium - Wellcome Strategic Awards [091911, 107457]
- MRC/EPSRC/BBSRC
- Cancer Research UK [C57744/A22057]
- Leverhulme Trust [RPG-2018-443]
- BBSRC [BB/P026354/1] Funding Source: UKRI
- EPSRC [EP/S004459/1] Funding Source: UKRI
- MRC [MC_UU_12010/1, MC_U137884181, MC_PC_15060, G0501975, MC_UU_00008/9, MC_UP_1201/15, G1000800, MR/K01577X/1, G0800158, MC_PC_16082, MC_UU_00008/1, MC_PC_15002] Funding Source: UKRI
- Cancer Research UK [22057] Funding Source: researchfish
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Cytoskeletal actin dynamics is essential for T cell activation. Here, we show evidence that the binding kinetics of the antigen engaging the T cell receptor influences the nanoscale actin organization and mechanics of the immune synapse. Using an engineered T cell system expressing a specific T cell receptor and stimulated by a range of antigens, we found that the peak force experienced by the T cell receptor during activation was independent of the unbinding kinetics of the stimulating antigen. Conversely, quantification of the actin retrograde flow velocity at the synapse revealed a striking dependence on the antigen unbinding kinetics. These findings suggest that the dynamics of the actin cytoskeleton actively adjusted to normalize the force experienced by the T cell receptor in an antigen-specific manner. Consequently, tuning actin dynamics in response to antigen kinetics may thus be a mechanism that allows T cells to adjust the lengthscale and timescale of T cell receptor signaling.
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