Key result
Engagement of ICAM-1 caused MTOC polarization at a higher frequency in HTLV-1-infected cells, whereas polarization induced by CD3 or CD28 antibodies was inhibited by HTLV-1 infection.
Engagement of ICAM-1 on HTLV-1-infected T cells promotes MTOC polarization and viral gene expression, facilitating virologic synapse formation.
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May facilitate HTLV-1 spread via virologic synapses; leaves open therapeutic targeting in humans.
Barnard et al. (2005) studied HTLV-1 infection. Antibodies to ICAM-1 (CD54), CD3, or CD28 was evaluated on Microtubule-organizing center (MTOC) polarization. Engagement of ICAM-1 caused MTOC polarization at a higher frequency in HTLV-1-infected cells, whereas polarization induced by CD3 or CD28 antibodies was inhibited by HTLV-1 infection.
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