Immobilized anti-TCR mAb induces split functions in a CD8+ CTL clone.

A signal through the T cell receptor (TCR) without a second costimulatory signal provided by antigen-presenting cell (APC) generally causes a state of anergy in CD4+ T helper (Th) 1 cells, but not in CD4+ Th2 cells. In contrast, less is known about anergic CD8+ T cells. We have examined whether a CD8+ cytotoxic T lymphocyte (CTL) clone incapable of producing IL-2 could be rendered into a state of unresponsiveness by treatment with immobilized anti-TCR mAb in the absence of a secondary stimulation. The CD8+ CTL clone was induced into nonproliferative response to subsequent antigen stimulation while it was bound to immobilized anti-TCR mAb. The immobilized anti-TCR mAb-treated CTL clone also failed to significantly produce cytokine with antigen stimulation. In contrast, the ability of the CTL clone to specifically lyse target cells was apparently retained. The results suggest that there might be intracellular signal pathways via the TCR for CTL functions such as proliferative response, cytokine production, and CTL killing.