Abstract
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) |
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Pages (from-to) | 317-325 |
Number of pages | 9 |
Journal | Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology |
Volume | 11 |
Issue number | 4 |
State | Published - 1996 |
Externally published | Yes |
Keywords
- Apoptosis
- CD2
- CD3
- Human T lymphotropic virus type I
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Virology