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Effect of methotrexate on the immune response in children with acute lymphatic leukaemia
Lymphocyte count, lymphocyte subpopulations identified by monoclonal antibodies and mitogen stimulation assays with phytohaemagglutinin, concanavalin A, pokeweed mitogen and staphylococcal protein A, were used to quantitate the effect of methotrexate on the immune response in children with acute lymphatic leukaemia on maintenance therapy. Methotrexate exerted a profound but apparently short-term effect on these parameters as it is prescribed in current maintenance schedules for childhood acute lymphatic leukaemia. A significant drop in lymphocyte count, affecting all subpopulations, was observed 4 h after oral or intramuscular administration of methotrexate which had reverted to pre-methotrexate values one week after the drug was given. Lymphocyte function was markedly affected, with a major decrease in mitogen responsiveness 1 h after methotrexate and a reversion to pre-methotrexate values by 48 h. A selectivity of suppressor T cells to methotrexate is proposed as being responsible for early recovery. Scheduling of methotrexate in current maintenance programmes would therefore appear to allow adequate time for recovery of immunoresponsiveness between doses.
Lymphocyte count, lymphocyte subpopulations identified by monoclonal antibodies and mitogen stimulation assays with phytohaemagglutinin, concanavalin A, pokeweed mitogen and staphylococcal protein A, were used to quantitate the effect of methotrexate on the immune response in children with acute lymphatic leukaemia on maintenance therapy. Methotrexate exerted a profound but apparently short-term effect on these parameters as it is prescribed in current maintenance schedules for childhood acute lymphatic leukaemia. A significant drop in lymphocyte count, affecting all subpopulations, was observed 4 h after oral or intramuscular administration of methotrexate which had reverted to pre-methotrexate values one week after the drug was given. Lymphocyte function was markedly affected, with a major decrease in mitogen responsiveness 1 h after methotrexate and a reversion to pre-methotrexate values by 48 h. A selectivity of suppressor T cells to methotrexate is proposed as being responsible for early recovery. Scheduling of methotrexate in current maintenance programmes would therefore appear to allow adequate time for recovery of immunoresponsiveness between doses.