The Journal of Immunology, 1963, 91: 761-770.
Copyright © 1963 by The American Association of Immunologists, Inc.
Enhanced Antitoxin Responses in Irradiated Mice Elicted by Complexes of Tetanus Toxoid and Specific Antibodya
Richard D. Stoner and
Geronimo Terresb
From the Medical Research Center, Brookhaven National Laboratory, Upton, L. I., New York and the Department of Physiology, Stanford University, Stanford, California
Abstract
- 1. Enhanced primary antitoxin responses were obtained in mice immunized by intravenous injection with complexes of tetanus toxoid and mouse antitoxin presumably formed either in vivo or prepared in vitro in antigen-antibody ratios of antibody excess, equivalence and antigen excess.
- 2. The demonstration of the enhancement phenomenon elicited by complexes of toxoid and isologous mouse antitoxin provide conclusive evidence that the antibody portion of the complex does not need to be of heterologous origin in order to elicit enhanced primary antibody responses in mice.
- 3. Intravenous immunization with the above complexes elicited enhanced primary responses in irradiated animals, whereas minimal responses were obtained with antigen only.
- 4. Little difference was observed in primary responses in nonirradiated mice when antigen only or antigen complexed with specific antibody was given by subcutaneous injection. However, enhanced primary antitoxin responses were obtained in irradiated mice (400 rads) immunized with the various complexes over the responses observed in irradiated animals immunized with antigen only. The greatest degree of enhancement occurred when the complexes were prepared in the region of equivalence and antigen excess.
- 5. Secondary antitoxin responses were repressed when the same complexes of antigen and antibody were injected to elicit secondary responses. A corresponding repression of secondary responses was observed in irradiated mice when radiation doses of 300 rads were delivered 24 hr before the second injection of antigen complexed with specific mouse antitoxin.
Footnotes
a Research supported by the U. S. Atomic Energy Commission and by Grant E-3733 from the U.S. Public Health Service.
b U.S. Public Health Service Research Career Development Awardee (GM-K3-5794-C1).
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