Regulation of the antibody response to type 3 pneumococcal polysaccharide. IV. Role of suppressor T cells in the development of low-dose paralysis.
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Biomedical subjects
Publications and source records attributed to B Prescott.
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The effect of treatment with antilymphocyte serum (ALS) on the magnitude of the plaque-forming cell (PFC) response to Type III pneumococcal polysaccharide (SSS-III) was assessed in athymic nude mice and thymus-bearing littermate controls. Without ALS treatment, the PFC response was slightly higher in nude than in control mice. Treatment with ALS had no effect on the response of nude mice; however, considerable enhancement was noted in thymus-bearing controls. Such enhancement was ALS dose-dependent and demonstrable under conditions in which there was substantial inactivation of thymic-derived "helper" cells required for an antibody response to erythrocyte antigens. These findings suggest that amplifier and suppressor cells, which have been reported to regulate the magnitude of the antibody response to SSS-III, represent populations of thymic-derived cells (T cells) that are not present in nude mice. The activities of "helper" T cells and regulatory T cells appear to be independent of one another and mediated by separate subpopulations of T cells.
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Mycoplasma hyorhinis organisms were fractionated into lipid, carbohydrate, and protein fractions by chemical and physiochemical procedures. When all fractions were tested for complement fixation and inhibition of growth inhibition activity, only the protein fractions possessed activity. Thus, it appears that the major antigenic component of M. hyorhinis is a protein.
Parent bacteria and L-forms of some streptococci of group A, group D, and Streptococcus MG share common antigens as shown by cross-reactivity in growth inhibition, complement fixation, and Ouchterlony tests. Cross-reactivity between these streptococci or their L-forms with a staphylococcal L-form, or Mycoplasma pneumoniae, was found only rarely and only in low-titer complement fixation tests. Removal of all three serological reactivities from positive antisera by addition of chloroform-methanol (7:3) extracts of the streptococci or their L-forms, and failure to remove activities by protein extracts, indicated the glycolipid nature of the cross-reacting antigenic determinants.
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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.
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The glycolipid haptens of Mycoplasma pneumoniae became immunogenic when bound to membrane proteins of Acholeplasma laidlawii by reaggregation. This process consisted of the solubilization of lipid-depleted A. laidlawii membranes and M. pneumoniae glycolipids in 20 mm sodium dodecyl sulfate and dialysis of the mixed solutions against 20 mm Mg(2+). The antibodies produced in rabbits to the reaggregated glycolipids inhibited the metabolism of M. pneumoniae, fixed complement with M. pneumoniae glycolipids or whole cells, precipitated M. pneumoniae glycolipids, and agglutinated M. pneumoniae cells. All these antibody activities could be blocked or absorbed by the purified glycolipids but not by a series of carbohydrates containing glucose and galactose. It was concluded that the antiserum to the reaggregated glycolipids may be regarded as a specific serum to membrane glycolipids of M. pneumoniae, since the antibodies to A. laidlawii membrane proteins, present in this serum, did not react with the glycolipids or with any other cell component of M. pneumoniae.
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