Immunological Tolerance to Microbial Antigens II. Suppressed Antibody Plaque Formation to Shigella Antigen by Spleen Cells from Tolerant Mice

Abstract

Friedman, Herman (Albert Einstein Medical Center, Philadelphia, Pa.). Immunological tolerance to microbial antigens. II. Suppressed antibody plaque formation to Shigella antigen by spleen cells from tolerant mice. J. Bacteriol. 92:820–827. 1966.—An indirect, localized, antibody plaque procedure has been used to demonstrate a marked difference in the number of antibody plaques formed with spleen cell suspensions from normal and Shigella -tolerant mice. Whereas challenge with soluble Shigella antigen (SSA) into normal mice, ranging in age from 4 to 40 weeks, resulted in a rapid rise in antibody plaque formation to Shigella -treated sheep erythrocytes, there was only a slight increase in plaque formation with spleen cell suspensions from similarly challenged mice which had been made tolerant to Shigella antigen during neonatal life. Apparently, the suppression of plaque formation to Shigella in tolerant animals was specific, since both Shigella -tolerant and normal mice responded equally well to untreated sheep red blood cells after challenge with sheep erythrocytes only. Spleen cells from nonchallenged Shigella -tolerant mice did not form significant numbers of antibody plaques to SSA-treated red blood cells during an observation period of 4 to 30 weeks after neonatal administration of antigen. “Nonspecific” increases in plaque formation to untreated sheep red cells occurred with spleen cell suspensions from both normal and SSA-tolerant mice after challenge injection with Shigella antigen, with or without sheep erythrocytes. Such a response suggested an adjuvant effect for the endotoxin-containing Shigella antigen even in mice tolerant to the agglutinogenic moiety of SSA. The results of these experiments support the view that specific antibody-forming cells are either absent or in low number in lymphoid tissue from mice specifically tolerant to Shigella antigens. It seems unlikely that the low postchallenge agglutinin titers of tolerant mice are due to suppressed antibody formation by normal numbers of individual antibody-producing cells, or due to “masking” of normal antibody production by persisting circulating antigen.