Selective suppression of primary IgM responses by induction of low dose paralysis to type III pneumococcal polysaccharide.
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Biomedical subjects
Publications and source records attributed to H Braley-Mullen.
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Mice primed with a thymus-dependent form of Type 3 pneumococcal polysaccharide (S3), i.e. S3 coupled to erythrocytes (S3-RBC) produces S3-specific IgG antibody after secondary challenge with S3-RBC. When mice are depleted of T cells by treatment with anti-lymphocyte serum (ALS) at the time of priming, no IgG antibody is produced after secondary challenge. In order to determine the cellular basis for this phenomenon, various combinations of T and/or B cells from ALS-treated or normal primed mice were transferred to irradiated recipients prior to secondary challenge with S3-RBC. The results indicated that T cells were required at the time of priming with S3-RBC in order to (a) prevent the induction of tolerance in S3-specific B cells in mice primed with high doses of S3-RBC, and (b) induced differentiation of IgG-producing B cell precursors to Bgamma memory cells in mice primed with low doses of antigen.
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Mice primed with a thymus- (T) dependent form of Type III pneumococcal polysaccharide (S3), i.e., S3 coupled to erythrocytes (S3-RBC) produce S3-specific IgG antibody after secondary challenge with either S3 or S3-RBC. The production of IgG antibody by mice challenged with S3 was shown to be T independent since secondary responses were enhanced when mice were treated with anti-lymphocyte serum (ALS) at the time of secondary challenge with S3 and T-depleted spleen cells responded as well as unfractionated spleen cells to S3 in an adoptive transfer system. Secondary S3-specific IgG responses in mice challenged with S3-RBC were shown to be T dependent by the same criteria. The results obtained by using S3 as the antigen indicate that IgG-producing B cells (B lambda cells) can recognize and respond to antigen in the absence of helper T cells. On the other hand, T cells were required for the induction of S3-specific memory B lambda cells since mice depleted of T cells by treatment with ALS at the time of priming with S3-RBC failed to produce S3-specific IgG antibody after secondary challenge with either S3-specific IgG antibody after secondary chall-nge with either S3 or S3rbc. Since RBC-specific memory cells were induced in T-deprived mice the results suggest that T cell regulation of IgG antibody production may vary for different antigens.
Twenty-seven of 30 Strain 2 guinea pigs immunized with 100 mug guinea pig thyroglobulin (GPTG) prepared either from Hartley (H) or Strain 13 (13) thyroids developed experimental autoimmune thyroiditis (EAT) whereas only 1 of 39 similarly immunized Strain 13 guinea pigs developed EAT. F1 hybrids behaved like the Strain 2 parent in that 16 of 20 developed EAT. The susceptible Strain 2 and F1 guinea pigs had higher hemagglutinating antibody titers to GPTG than the Strain 13 guinea pigs whereas all three strains had similar delayed skin reactivity to GPTG. The results suggest that susceptibility of guinea pigs to thyroiditis is genetically controlled and that production of antithyroglobulin antibody may be important in determining disease susceptibility.
Mice primed with a thymus- (T)3 dependent form of Type III pneumococcal polysaccharide (S3), i.e., S3 coupled to sheep or horse erythrocytes (S3-RBC), produce S3-specific IgG antibody after secondary challenge with either the T-dependent (S3-RBC) or T-independent (S3) form of the antigen. The potential to produce IgG antibody after challenge with S3-RBC appears earlier after priming than the potential to produce IgG after challenge with S3, suggesting that different "memory" cells may be involved in the two responses. The "memory" cells were shown to be S3-specific since S3 had to be present on the carrier in order for priming to occur and carrier specificity was not required for elicitation of the secondary response by S3-RBC.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.