The nature of the IgA deficiency in epileptic patients during anticonvulsant therapy was investigated. First, circulating T and B cells were assessed by surface markers in 10 epileptic patients and in a patient with primary IgA deficiency. The number of surface IgA bearing cells was within normal range, which suggested that the defects were present on the terminal differentiation of B cells. Therefore, the capacity of differentiation into immunoglobulin(Ig) producing cells was studied by lymphocyte cultures with pokeweed mitogen(PWM) stimulation. Cytoplasmic Ig was stained by immunofluorescence technique and the release of Ig into the culture supernatant was determined by radioimmunoassay. The results indicated that there were two groups according to the defects observed. The first group, consisting of 2 epileptic patients, showed IgA synthesis in cytoplasma without any release of IgA into the supernatant. The second group, comprised of 8 epileptic patients and a primary IgA deficiency patient, was found to fail to synthesize IgA. Thus, the IgA deficiency in these patients is seem to be a heterogeneous disease caused by at least two different defects in the process of the terminal differentiation of B cells.
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