Abstract
A baculovirus-expressed chimeric recombinant IgG 1 (rIgG 1) antibody, with Cγ 1 and Cκ human constant domains, was derived from the murine monoclonal antibody (mAb) 13B8.2, which is specific for the CDR3- like loop of the CD4 molecule and which inhibits HIV-1 replication. Chimeric rIgG 1 antibody 13B8.2 blocked, in a dose-dependent manner, antigen presentation through inhibition of subsequent IL-2 secretion by stimulated T cells. The one-way mixed lymphocyte reaction was abrogated by previous addition of baculovirus-produced rIgG 1 13B8.2 in the T-cell culture. Anti-proliferative activity of rIgG 1 was demonstrated on CD3-activated CD4 + T lymphocytes from healthy donors, such effect being associated with reduced IL-2 secretion of activated T cells. On the other hand, no proliferation inhibition was observed on CD4 + T lymphocytes activated with phorbol ester plus ionomycin, suggesting that rIgG 1 13B8.2 preferentially acts on a proximal TCR-induced signaling pathway. Treatment of DBA1/J human CD4-transgenic mice with 100 μg of recombinant antibody for three consecutive days led to in vivo recovery of rIgG 1 antibody 13B8.2 both coated on murine T lymphocytes and free in mouse serum, without CD4 depletion or down-modulation. These findings predict that the baculovirus-expressed chimeric rIgG1 anti-CD4 antibody 13B8.2 is a promising candidate for immunotherapy.
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