PRODUCTION OF A RUNTING SYNDROME AND SELECTIVE γA DEFICIENCY IN MICE BY THE ADMINISTRATION OF ANTI-HEAVY CHAIN ANTISERA

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Abstract
Conventional Swiss mice were treated from birth with intraperitoneal injections of anti-immunoglobulins in an attempt to create an experimental dysgammaglobulinemia. Mice treated with anti-gammaM were immunologically suppressed in all immunoglobulin classes as determined by serum antibody titers, splenic plaque-forming cells, serum immunoglobulin levels, and immunofluorescent analysis of plasma cells in lymphoid tissues. Treatment immediately after birth with high concentrations of anti-gammaM leads to a developmental arrest characterized by severe immunosuppression, failure to gain weight, and premature death. The pathogenesis of anti-gammaM runting syndrome is unknown. Animals similarly treated with anti-gammaG, anti-gammaA, or control normal goat or rabbit gamma-globulins developed normally. The frequency of occurrence and severity of anti-gammaM-induced runting syndrome is dependent upon the concentration of anti-gammaM-globulin administered. Administration of anti-gammaA resulted in a selective gammaA deficiency that was characterized by a marked reduction in serum-gammaA and an absence of gammaA-containing cells in the spleen. However, essentially normal numbers of plasma cells were found in the gastrointestinal lamina propria of anti-gammaA-treated animals concomitantly with suppressed levels of gammaA in intestinal fluids.