Abstract
CD66a (CEACAM1), an adhesion molecule that has regulatory function on T lymphocytes, was found to be expressed on a minority of mouse natural killer (NK) cells, especially in the liver. CD66a expression on NK cells depended on their differentiation stage, with highest levels on immature CD49b(-)NK cells. Expression of CD66a on NK cells was strongly enhanced by in vitro activation with interleukin-12 (IL-12) and IL-18. However, in vivo NK cell stimulation by infection with lactate dehydrogenase-elevating virus did not lead to strong CD66a expression, even on activated interferon--gamma-producing NK cells. These results indicate that CD66a expression is differently regulated, depending on the NK cell activation pathway, which may lead to distinct regulatory mechanisms of the functional subpopulations of these cells.