A successful immune response depends on the migration of lymphocytes into lymph nodes or inflamed tissues where they make contact with antigen‐presenting cells. We are interested in how one member of the integrin family, leukocyte function‐associated antigen‐1 (LFA‐1), controls the function and, in particular, the migration of immune cells. We find that this integrin operates not only as an adhesion receptor for T lymphoblasts (T cells) but also induces their migration in vitro at approximately 15 μm/min. Migration requires active myosin light chain kinase at the leading edge and Rho kinase at the trailing edge of the cell. Two active conformations of LFA‐1 are differently distributed on the T‐cell membrane and regulate independent aspects of migration. High‐affinity LFA‐1 is located in a midcell ‘focal zone’ and influences the speed of migration, whereas intermediate affinity LFA‐1 controls leading edge adhesions. Manipulating LFA‐1 conformation in vivo can be performed, for example, by creating the active conformation in a transgenic mouse, and this model gives further insight into the role of LFA‐1 in migration. In humans, the beneficial effect of functioning CD18 integrins in combating infections in vivo is illustrated by rare patients displaying two forms of leukocyte adhesion deficiency. In summary, we speculate that T cells have evolved a mode of rapid migration that is of paramount importance in achieving the high‐speed immune surveillance upon which depends the body’s protection against diverse invaders from pathogens to cancer cells.