Anti-CD26 monoclonal antibodies can reversibly arrest human T lymphocytes in the late G1 phase of the cell cycle.

Three different anti-CD26 monoclonal antibodies (mAbs) are described, which specifically inhibited proliferation of human T lymphocytes after stimulation with PHA, tetanus toxoid or soluble anti-CD3 mAb. Anti-CD26 mAbs induced in T cells a dose-dependent shift of the maximum of DNA synthesis, which was due to a transitory arrest of cells in the cell cycle. This cell cycle arrest was found to occur in the late phase of G1 since the expression of the T cell activation markers CD25-, CD71-, and HLA-DR-positive cells was the same in anti-CD26 mAb-containing and control cultures. Propidium iodide staining further confirmed the assumption that the arrest occurs in the first round of the cell cycle before S phase cells were detectable. Because the cells were arrested before consuming IL-2 in the S phase, we observed in accumulation of IL-2 in anti-CD26 mAb-containing cultures, whereas IFN-gamma production by PHA-activated T lymphocytes was reduced. These data indicate that CD26 is involved in the processes of T cell activation and proliferation.