Defective RNA Synthesis in Lymphocytes from Patients with Primary Agammaglobulinemia.

Addition of tetanus toxoid to sensitized lymphocytes from normal subjects and patients with "secondary" acquired agammaglobulinemia resulted in an increased incorporation of tritiated uridine into RNA and this increase was sustained for 48 to 72 hours in vitro. In contrast, the quantity of H(3)-uridine incorporated into the RNA of lymphocytes from patients with "primary" acquired agammaglobulinemia decreased after 48 hours of exposure to specific antigen. Lymphocytes from patients with primary agammaglobulinemia were also distinguished by their subnormal and poorly sustained response to phytohemagglutinin and to rabbit antiserum to Iymphocytes. These data suggest that the defect in primary agammaglobulinemia involves, either as a primary phenomenon or as a secondary event, an abnormality of quantitative RNA synthesis or of RNA stability in the circulating lymphocyte.