We demonstrate that CD2 receptor engagement, but not CD3 cross-linking, induces apoptosis in lymphocytes transformed by human T-cell lymphotropic virus type I (HTLV-I). Mitogenic pairs of anti-CD2 monoclonal antibodies inhibited [3H]thymidine incorporation from 25 to 62% in CD2+ HTLV-I- infected lymphocytes. This inhibition was associated with a 20-40% reduction in cell number and viability over a 3-day period, morphologic evidence of apoptosis, and irreversible DNA fragmentation. While cyclosporin A abrogated CD2-mediated proliferation in peripheral blood mononuclear cells, it had no effect on CD2-induced apoptosis in the HTLV-I-infected cell lines. Since HTLV-I is mitogenic to resting lymphocytes through CD2 activation pathways, these results suggest that HTLV-I-infected lymphocytes are primed for apoptosis following additional CD2 stimulation. This CD2-mediated apoptosis might be a factor in immune regulation of HTLV-I-associated diseases or might offer a novel adjunctive approach to treatment.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology|
|State||Published - 1996|
- Human T lymphotropic virus type I
ASJC Scopus subject areas
- Immunology and Allergy