Effective immune responses rely on the efficient migration of leukocytes. Yet, how temperature regulates migration dynamics at the single-cell level has remained poorly understood. Using zebrafish embryos and mouse tissue explants, we found that temperature positively regulates leukocyte migration speed, exploration, and arrival frequencies to wounds and lymph vessels. Complementary 2D and 3D cultures revealed that this thermokinetic control of cell migration is conserved across immune cell types, independently of the 3D tissue environment. By applying precise (sub-)cellular temperature modulation, we identified a rapid and reversible thermo-response that depends on myosin II activity. Small physiological increases in temperature (1 degrees C-2 degrees C), as present during fever-like conditions, profoundly increased immune responses by accelerating arrival times at lymphatic vessels and tissue wounds. These findings identify myosin-II-dependent actomyosin contractility as a critical mechanical structure regulating single-cell thermo-adaptability, with physiological implications for tuning the speed of immune responses in vivo.