The glycoprotein CD86 expressed on APCs provides a costimulatory signal nec
essary for an efficient activation of naive T cells. In contrast, there is
controversy about the condition of expression and the function of CD86 on T
cells, In this study, we have analyzed the phenotype and the biological ac
tivity of CD86(+) T cells generated from human PBMC. Results show that CD86
expression on T cells is induced by long term stimulation via CD3 and IL-2
R and is down-regulated as the cells become quiescent. The CD86-expressing
cells are memory effector T cells: 1) they express CD45RO and high levels o
f the activation markers CD25, CD54, and HLA-Dr; 2) they selectively expres
s CD30, CD40-ligand, and CD70; and 3) in response to stimulation, most of t
hem produce IFN-gamma before dying by apoptosis. We then analyzed whether C
D86 expressed on T cells is functional. Results show that paraformaldehyde-
fixed CD86(+) T cells enhance the proliferation and production of IFN-gamma
by anti-CD3 mAb-stimulated naive T cells and induce proliferation of resti
ng allogenic T cells. All these effects are prevented by neutralizing anti-
CD86 mAbs, In contrast, we report no autocrine effect of CD86 in CD86(+) T
cell activation, In conclusion, these data show that human memory effector
T cells express a functional form of CD86 that can costimulate naive T cell
responses.