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The increase in splenic plaque-forming cell (PFC) responsiveness which occurs in mice following the injection of a primary dose of 108 sheep red blood cells was measured using the spleen cell transfer system. As for grafts of normal spleen cells, the peak direct (19S) and indirect (7S) responses obtained with grafts of primed spleen cells were found to be related to the number of cells transferred in a near-parabolic fashion. Splenic direct PFC responsiveness as measured by the regression defining the corresponding graft-response relationship was increased about five times 4 weeks after priming; focus-forming capacity was also increased by a similar factor. At the same time indirect PFC responsiveness was increased almost twenty times. These results are discussed in terms of antigen-induced changes in the populations of PFC precursors and antigen-reactive auxiliary cells in the spleen. [ABSTRACT FROM AUTHOR]

Specific antibody formation by transferred cells from immunized donors has been demonstrated in adult recipients with cells derived from caecal tonsils, blood and peritoneal exudate as well as from spleen. Cells from all these sources formed both γM and γG antibody, regardless of whether the donors had received one or two injections of antigen. There was no difference in the amount of antibody formed by cells from primary or secondary donors. An autoradiographic method for detecting small amounts of primary 7S fowl antibody (which does not give passive haemagglutination reactions) is described. [ABSTRACT FROM AUTHOR]

We observed that the volume of any anti-HSA serum needed to bind 50 per cent of the antigen is a linear function of the amount of antigen present in the reaction mixture over three log units. The slope is characteristic of each anti- serum and reflects the ‘avidity’ of the antibodies. By using this quantitative index we found that the avidity of antibodies produced during the secondary adoptive response depends on the number of the cells transferred : few cells will produce antibodies of lower avidity than many cells. The dose of antigen given as a booster also influences the quality of the antibody produced; in the extreme case where some primed cells were rendered ‘tolerant’ by supra-optimal doses of challenging antigen, substantial amounts of low avidity antibodies were synthesized. The results can be explained by competition for antigen among competent cells, favouring those cells which carry antibody sites with high affinity for the corresponding antigenic determinant. [ABSTRACT FROM AUTHOR]

The in vitro cytotoxic effect of spleen cells of mice immunized by tumour allografts was studied by measuring target cell inactivation as a function of release of radioactive label (51 Cr) or loss of cloning efficiency. When sensitized lymphoid cells were incubated with target cells at a ratio of 100: 1, up to 90 per cent of the incorporated label was released within 6–9 hours, while the number of clone- forming cells was reduced by up to 99 per cent in the same time period. Isoantiserum from the graft recipients, as well as its 1 9S and 7S fractions, protected target cells against the toxic effect of the spleen cells, but a lipoprotein antigen isolated from the tumour cells failed to inhibit the cytotoxic reaction. Target cell lysis as measured by specific release of 51Cr was partially inhibited by actinomycin-D and by cycloheximide at concentrations which effectively blocked DNA! dependent RNA and protein synthesis.

Investigates the fate of CBA spleen cells transplanted into F[sub 1] adult host mice. Tracking of the donor cells by means of a chromosomal marker; Comparison of the results with graft-versus-host reaction; Occurrence of an early but short-lived burst of donor cell activity in the spleen; Cell proliferation.

Cytology and histology of recipients of allogeneic bone marrow were studied 13, 20, 24, 30 and 34 days after transplantation. The developing chronic secondary disease was characterized by increased numbers of myeloid cells, by lymphopenia and by erythroblastopenia in the bone marrow and the spleen. Erythroblastopenia together with lymphopenia and augmented myeloid cells also occurred in irradiated F1-hybrids suffering from a chronic homologous disease. The latter model eliminated the following as a cause of erythroblastopenia in secondary disease: (I) host-versus-graft reaction against donor-type erythroblasts for immunogenetical reasons, and (2) graft-versus-host reaction against recipient-type erythroblasts since they had already been destroyed by irradiation. Treatment of the donor with ALS iesulicd iii a suppression of homologous disease in F1-hybrids with a cytology resembling that of recipients of syngeneic spleen cells. The same treatment only delayed the onset of chronic secondary disease in recipients of allogeneic bone marrow. These allogeneic recipients, in contrast to the F1-hybrid recipients, died with the typical morphology of a chronic secondary disease. In recipients of syngeneic bone marrow from donors treated with ALS, repopulation with lymphocytes was somewhat delayed and transient erythroblastosis in the spleen occurred 20 days after transplantation. [ABSTRACT FROM AUTHOR]