T cell activation requires co-engagement of the TCR with accessory and cost
imulatory molecules. However, the exact mechanism of costimulatory function
is unknown. Mice lacking CD2 or CD28 show only mild deficits, demonstratin
g that neither protein is essential for T cell activation. In this paper we
have generated mice lacking both CD2 and CD28. T cells from the double-def
icient mice have a profound defect in activation by soluble anti-CD3 Ab and
Ag, yet remain responsive to immobilized anti-CD3, This suggests that CD2
and CD28 may function together to facilitate interactions of the T cell and
APC, allowing for efficient signal transduction through the TCR.