DEPLETION OF T-LYMPHOCYTES WITH IMMUNOTOXIN RETARDS THE PROGRESS OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN RHESUS-MONKEYS

FN18-CRM9 is an anti-rhesus anti-CD3 immunotoxin that call transiently deplete T cells to 1% of initial values in both the blood and lymph n ode compartments and can induce long-term tolerance to mismatched rena l allografts. We have investigated the ability of this immunotoxin to interdict the course of an experimental rhesus T-cell-driven autoimmun e disease, experimental allergic encephalomyelitis (EAE) induced by my elin basic protein. Monkeys showing CSF pleocytosis were then treated with FN18-CRM9 alone or in combination with cranial irradiation (325 o r 650 cGy). EAE in nontreated control monkeys progressed rapidly. Para lysis occurred 4-6 days after CSF pleocytosis. Paralysis was either de layed or never occurred in treated monkeys, and histopathology reveale d few inflammatory plaques that were notable for their low or absent T cell content. While T cells repopulate ill the periphery posttreatmen t, they do not return to the CNS in large numbers, suggesting that the newly repopulated T cells have lost their previously acquired CNS hom ing capability. Anti-CD3 immunotoxin may be useful in treating clinica l T-cell-driven autoimmune diseases such as rheumatoid arthritis and m ultiple sclerosis.