ABSTRACT
The IgM antibody response to Type III pneumococcal polysaccharide (SSS-III) was assessed in F(1), F(2), and backcross progeny derived from high (BALB/cAnN) and extremely low (CBA/HN) responding parental strains of inbred mice. The results of these studies indicated that a major component involved in the antibody response is X-linked, i.e., carried on the X chromosome; this component determines responsiveness to SSS-III in an almost quantal or "all-or-none" manner. Other factors, presumably autosomal genes, regulate the magnitude of the antibody response produced by mice possessing the X-linked gene; these appear to influence independently the number of antibody-producing cells found after immunization and the amount of antibody made by such cells. Strains of inbred mice varied widely in their ability to respond to SSS-III. Responsiveness was not associated with H-2 histocompatibility type. The implications of these findings with respect to the genetic control of the antibody response to SSS-III are discussed.
Subject(s)
Antibody Formation , Antibody-Producing Cells , Immunogenetics , Polysaccharides, Bacterial , Sex Chromosomes , Animals , Antibodies/analysis , Antigens, Bacterial , Crosses, Genetic , Erythrocytes/immunology , Escherichia coli/immunology , Female , Hemolytic Plaque Technique , Immunoglobulin M/analysis , Male , Mice , Mice, Inbred Strains , Sheep/immunology , Streptococcus pneumoniae/immunologyABSTRACT
CBA/N mice fail to respond to T-independent antigens, and give a diminished response to T-dependent antigens. The cellular basis of the diminished response to T-dependent antigens in this strain was analyzed by means of adoptive transfers of various primed cell populations along with cells from the immunologically normal, histocompatible strain CBA/CaJ. CBA/N mice behaved normally as recipients and had normal levels of spleen helper cell activity. However, CBA/N spleen cells, used as a B cell source, produced only 56% as much antibody as CBA/CaJ cells. Since CBA/N mice have a relative frequency of immunoglobulin-bearing lymphocytes roughly half that of normal mice, these results suggest that CBA/N mice have a quantitative defect in spleen B cells responsive to T-dependent antigens.