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Effects of Pneumococcus Capsular Polysaccharides on the Degradation of Rabbit Antibodies in Mice¹

From the Department of Pediatrics, Harvard Medical School and the Children's Hospital Medical Center, Boston, Massachusetts

Abstract

Mice injected intraperitoneally with potentially immunizing and immunologically paralyzing doses of pneumococcus type II, III and XII polysaccharides were subsequently given radioiodinated rabbit antibodies intravenously and the disappearance of the labeled proteins from these mice was studied. It was found that:

1. The degradation of rabbit antibodies specific for a given polysaccharide followed a triphasic disappearance pattern when injected into mice that had received 500 µg of that polysaccharide even 35 days earlier. this behavior was attributable directly or indirectly to specific interaction of the antibodies with the antigen.

2. The interaction of rabbit antibodies with specific polysaccharide in vivo accelerated the formation of antibodies against rabbit -globulin by the mouse.

3. Rabbit antibodies when mixed with their specific polysaccharides prior to injection also accelerated the formation of antibodies to rabbit -globulin by the mouse. Rabbit antibodies in complexes formed with specific polysaccharide in the zone of antigen excess and immediately injected into mice disappeared, as did rabbit antibodies in mice given 500 µg of homologous polysaccharide.

4. Small or immunizing doses of polysaccharide had no apparent effect on the metabolism of rabbit antibodies given 35 days later, whether the antibodies were specific for the polysaccharide or not.

These studies suggest that the specific immunological paralysis induced in mice by pneumococcus polysaccharide is not due to continuous neutralization of antibodies by tissue-fixed polysaccharide.

Footnotes

Supported by a grant (A 251) from the National Institute of Arthritis and Metabolic Diseases, United States Public Health Service. Presented in part before the Society for Pediatric Research, Atlantic City, New Jersey, May 8–9, 1958.

² Established Investigator, American Heart Association.

³ This work was done during tenure of a Guggenheim Fellowship, 1958.