Elastohydrodynamics and Kinetics of Protein Patterning in the Immunological Synapse
Fig 1
(a) Sketch of the interaction between a T-lymphocyte cell (T-cell) and a supported antigen-seeded bilayer.
The two membranes are separated by transmembrane receptors bound to ligands in the bilayer. (b) Close-up schematic view of the synaptic cleft formed between the T-cell membrane and the glass supported bilayer. The cell membrane has a thickness b ≈ 8 nm and the membrane gap height is given by h = h(x, y, t). The trans-membrane receptors form bonds with the ligands in the bilayer with lengths and concentrations, TCR − pMHC ≈ 15 nm, C1(x, y, t), and LFA − ICAM ≈ 45 nm, C2(x, y, t). During protein bond formation and depletion, the cell membrane deforms generating a viscous flow u(x, y, z) in the membrane gap. The flow generates a viscous frictional force Fμ parallel with the glass supported bilayer that acts on the cell membrane and the transmembrane proteins and thus affects their motion. Any deformation of the membrane generates a restoring elastic bending force FB, while the deformation of the TCR-pMHC and LFA-ICAM bonds generates a spring force Fκ.