T-Cell Mechanosensation & Fate Simulator

Live Motor-Clutch & Nuclear Mechanotransduction

Retrograde Flow: 42.0 nm/s

Integrin Clutches: Catch State

Nuclear TCF1: 78.5%

Nuclear YAP/TAZ: 21.5%

Cytoskeletal Tension 18.4 pN Focal adhesion transmitted load

Memory Precursor Prob (TCM) 82.0% CD62L+ TCF1+ self-renewal

Short-Lived Effector (SLEC) 18.0% KLRG1+ Blimp-1+ terminal

TCF1 / FoxO1 Accumulation 78.5% Quiescence & stemness driver

Biophysical Tuners

Substrate Elasticity (E) 1.5 kPa

TCR Affinity / Antigen Density High (120/µm²)

Actin Polymerization Rate 42 nm/s

Blebbistatin (Myosin II Inhibitor) 0.0 µM

Predominant Lineage Central Memory T Cell (TCM)

TCM: 82% SLEC: 18%

Mechanobiology Mechanism

In soft lymph nodes (0.5–2.0 kPa), balanced motor-clutch tension maintains optimal integrin engagement without excessive nuclear flattening. This permits nuclear retention of TCF1 & FoxO1, driving self-renewing memory precursor (TCM) programs.

In stiff or fibrotic microenvironments (>25 kPa), high cytoskeletal stress stretches nuclear pores, prompting YAP/TAZ & Blimp-1 nuclear translocation that irreversibly commits T-cells toward short-lived effector (SLEC) states.