Antigen-driven shedding of L-selectin from human gamma delta T cells.

Activation of lymphocytes leads to the modulation of a number of surface molecules. We have investigated the expression of one such molecule. L-selectin, following activation of gamma delta T cells with Mycobacterium tuberculosis. L-selectin is modulated during lymphocyte entry into lymph nodes; this modulation reflects the recirculation and homing potential of lymphocytes. We find that stimulation of gamma delta T cells by M. tuberculosis antigens results in shedding of L-selectin from gamma delta T cells. Re-expression of L-selectin occurs on removal of antigen suggesting that the regulation of expression is controlled by the presence or absence of antigen. The gamma delta T-cell receptor (TCR)-positive, L-selectin negative population of peripheral blood lymphocytes appears to be resting cells, as assessed by forward- and light-scatter analysis. We further find that gamma delta T cells isolated from a site of infection, the pleural fluid of a tuberculosis patient, are L-selectin negative, and that L-selectin is re-expressed following culture of the pleural fluid gamma delta T cells in the absence of antigen. These results demonstrate that, in addition to stimulation with polyclonal mitogens, antigen stimulation can also promote the surface shedding of L-selectin and that gamma delta T cells have the potential to home to sites of infection supporting their role in the immunological defence against infectious micro-organisms.