Alessandro Moretta , Giuseppe Pantaleo

Monoclonal antibodies (mAb) directed to the molecular complex (formed by T3 molecules and by molecules carrying clonotypic determinants) serving as receptor for antigen on human T cells can induce cell activation, possibly leading to interleukin 2 (IL-2) release and cell proliferation (1, 2). However, although antibodies directed to the monomorphic T3 molecules induce polyclonal T cell responses, antibodies specific for the clonotypically restricted structures (termed Ti) only trigger cells bearing the relevant" clonotype (3). As a consequence, the functional effect(s) of anti-Ti mAb have been studied exclusively in cells belonging to the corresponding T cell clones (used for immunization). It is conceivable, however, that resting peripheral T cells carrying a given clonotype may be susceptible to triggering by the corresponding anticlonotypic antibodies and undergo proliferation. In this report we show that three mAb (designated JTil_3), originally raised against the clonotypic structure of a cloned variant of the IL-2-producing Jurkat leukemia cell line (designated JA3) (4, 5), and crossreacting with 0.5-1% of peripheral blood (PB) lymphocytes, promote (late) proliferation of PB T lymphocytes. This proliferation mostly reflects the expansion of clonotype-positive (JTi +) T cells that express either the T4 + or the T8 + phenotype. The antibody-stimulated JTi ÷ PB populations express disulphidelinked heterodimeric surface molecules similar to those of JA3 cells.