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Inhibition of OKT3 induced T4 and T8 cell proliferation by anti-Ia and anti-LFA-1 antibodies

Conference · · Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
OSTI ID:7024882

Monoclonal antibodies (Mab) directed at the CD3 molecule induce accessory cell (AC) dependent T cell proliferation. The role of AC in anti-CD3 induced proliferation is unclear but involves more than Fc receptor mediated crosslinking since Fc receptor (-) endothelial cells (EC) are effective AC for OKT3 induced proliferation. The role of AC in anti-CD3 induced proliferation was investigated by examining the ability of Mab directed at T cell and AC surface molecules to block OKT3 induced proliferation. AC-depleted T4 or T8 cells were used as responders. Monocytes (M phi), or EC, were used as AC. The Mab used included OKT4 and OKT8, 60.3, directed at the B subunit of LFA-1, MO-1 and the p150,95 protein, and L243, an anti-HLA-DR Mab. M phi-supported OKT3-induced proliferation was inhibited by 60.3, L243, and OKT4 but not OKT8. M phi-supported OKT3-induced proliferation of T8 cells was inhibited by OKT8, 60.3, and L243 but not OKT4. Much of the inhibition of T4 and T8 cell proliferation could be reversed by IL-2. L243 did not inhibit OKT3-stimulated T4 cell proliferation supported by Ia(-) EC. Moreover, neither L243 nor 60.3 inhibited AC independent stimulation of T4 cells by the combination of phorbol myristate acetate (PMA) and OKT3 or calcium ionophore and PMA. Thus, M phi support of OKT3-induced T8 and T4 cell proliferation involves recognition of Ia and an interaction involving the molecule identified by 60.3. These interactions may be necessary to promote optimal IL-2 production and thus maximal proliferation.

Research Organization:
UTHSCD, Dallas, TX
OSTI ID:
7024882
Report Number(s):
CONF-8604222-
Journal Information:
Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States), Journal Name: Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States) Vol. 45:4; ISSN FEPRA
Country of Publication:
United States
Language:
English