In vitro correction of the interleukin 2 defect of autoimmune mice

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Abstract
The effect of concanavalin A (Con A) and/or phorbol myristate acetate (PMA) on interleukin 2 (IL2) production and tritiated thymidine incorporation was measured in young (6 weeks) and old (16-24 weeks) autoimmune mice by pulsing 5 × 106 unfractionated spleen cells with 5 μg of Con A and/or 5 ng of PMA for variable periods of time. The apparent deficiency in Con A-stimulated IL2 production manifested by mice prone to the development of autoimmune disease was repaired by the addition of PMA. PMA did not enhance interleukin 1 (IL 1) secretion in autoimmune MRL-lpr mice either alone or in combination with Con A. The addition of purified IL 1 to Con A-pulsed autoimmune cells did not increase IL2 production. Freeze-thaw experiments suggested that PMA does not promote IL2 synthesis. Con A-pulsed cells plus PMA-pulsed cells do not syngergize. These data indicate that autoimmune-prone mice are capable of producing IL 2 and of proliferating in response to Con A provided the comitogen PMA is present. It can be argued that the failure to produce IL2 or to respond to proliferative signals is not fundamental to the development of the disease sustained by autoimmune-prone mice.