CD5 is expressed on thymocytes, all mature T cells, and a subset of mature
B cells, and probably contributes to T-cell-B-cell adhesion. We assessed wh
ether CD5-crosslinking by mAb augments T-cell stimulation. Plate-bound anti
-CD5 or anti-CD3 mAb alone had no effect on any of the assessed activation
parameters of resting T cells. However, concomitant signaling through both
CD5 and CD3 by plate-bound antibodies resulted in marked increases in T-cel
l surface CD69 expression and T-cell metabolism, as assessed by the T cell'
s ability to reduce 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxylmethoxyphenyl
)-2-(4-sulphophenyl)-2H-tetrazolium (MTS) to formazen. In addition, simulta
neous cross-linking of CD5 and CD3 caused a significant (p < 0.001) increas
e in phosphatidylinositol hydrolysis in resting T cells compared to stimula
tion with anti-CD3 mAb alone or anti-CD3 mAb plus anti-CD5 isotype control
antibody. These results indicate that CD5 augments signaling through CD3 an
d consequently functions as a costimulatory molecule for resting T cells.