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The affinity of anti-hapten antibodies, produced by single cells, was studied by hapten inhibition of plaque-forming cells using the local hemolysis in gel assay. The shift in affinity of anti-hapten antibodies, that occurs with time after immunization, was parallelled by an analogous shift, at the cellular level, with regard t o indirect plaque-forming cells (PFC). Thus, there was a gradual decrease of the hapten concentration which was needed t o suppress indirect plaque formation with time after immunization, indicating a gradual increase in the number of high affinity cells. No such shift was observed with cells causing direct plaque formation.Analogous studies were performed with hapten-specific antigen-binding cells of T and B origin by using hapten-inhbition of rosette-forming cells. Hapten-specific antigen-binding cells were present in both cell populations. Lymphocyte binding of haptenated red cells could be specifically inhibited by free hapten.It was found that antigen-binding B lymphoid cells became gradually more susceptible t o hapten inhibition with time after immunization, whereas no such change was observed in antigen-binding T lymphoid cells. Possible reasons for this discrepancy are discussed, as well as the implications for these findings regarding the specificity and structure of the T cell receptors.
The affinity of anti-hapten antibodies, produced by single cells, was studied by hapten inhibition of plaque-forming cells using the local hemolysis in gel assay. The shift in affinity of anti-hapten antibodies, that occurs with time after immunization, was parallelled by an analogous shift, at the cellular level, with regard t o indirect plaque-forming cells (PFC). Thus, there was a gradual decrease of the hapten concentration which was needed t o suppress indirect plaque formation with time after immunization, indicating a gradual increase in the number of high affinity cells. No such shift was observed with cells causing direct plaque formation.Analogous studies were performed with hapten-specific antigen-binding cells of T and B origin by using hapten-inhbition of rosette-forming cells. Hapten-specific antigen-binding cells were present in both cell populations. Lymphocyte binding of haptenated red cells could be specifically inhibited by free hapten.It was found that antigen-binding B lymphoid cells became gradually more susceptible t o hapten inhibition with time after immunization, whereas no such change was observed in antigen-binding T lymphoid cells. Possible reasons for this discrepancy are discussed, as well as the implications for these findings regarding the specificity and structure of the T cell receptors.
Injection into mice of a free reactive form of the hapten (4-hydroxy-3,5-dinitrophenyl)acetyl (NNP), induces a state of specific unresponsiveness to the hapten, upon its challenge with thymus-cependent and independent carriers. This unresponsiveness is maintained in vitro. Both induction and expression of the unresponsive state were found to be independent of T cells. Analysis of the mechanisms responsible for the B cell "tolerance" demonstrated that the major cause of unresponsiveness in this system is the blockade of specific surface receptors on B cells by the hapten, abolishing the focusing function of these receptors. "Tolerant" B cells, though they were unresponsive to the antigen, could be activated to anti-hapten antibody secretion by the B cell mitogen lipopolysaccharide (LPS), which does not require Ig-mediated binding. They also became fully responsive to the antigen NNP-LPS in specific thymus-independent responses after 24 hours of in vitro incubation in the absence of tolerogen, conditions which allow "deblocking" of Ig surface receptors, and, thus, restoration of the focusing function of these receptors. These results demonstrate that great care is required for a clearcut definition of B cell tolerance. In this example, the tolerant B cells were perfectly responsive to a competent ligand, and no indication of an altered triggering or effector processes was found. It appears that in this, as in many other cases of B cell tolerance, the systems or the animals are tolerant, whereas B cells maintain a resting nonactivated state and are fully responsive to the triggering signal. Thus, the existence of tolerance-inducing signals resulting in B cell unresponsiveness is questioned.
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