Hybridomas that produce two monoclonal antibodies (MoAbs) to salmon somatotropin (SST) and two MoAbsto salmon prolactin (SPRL) were established. Two MoAbsto SST, designated KM166and KM167, reacted specifically with SST and did not react with SPRL, proteins derived from host Escherichia coli, or bovine serum albumin. KM200and KM212raised against SPRLwere specific for SPRL. Using these MoAbswe have developed a sandwich-type enzyme immunoassay (ELISA) system for SST or SPRL. With these assays, SST and SPRLcould be quantitatively measured in the range of 0. 16~4 /ig/ml and 3. 1~200 yUg/ml, respectively. The immunoaffinity column using KM200adsorbed specifically SPRL. By elution with 7m urea/1 MNaCl, the SPRL was
The role(s) of helper T lymphocytes in preventing or altering tolerance induction in DNP-specific B lymphocytes was studied. As DNP-reactive helper T cells were reactive against the DNP-portion of the DNP-D-GL molecule, we could probe definitively the physiological role of helper T cells in preventing tolerance induction in B lymphocytes by DNP-D-GL. The results demonstrated that the induction of DNP-specific B cell tolerance by DNP-D-GL can be completely prevented by the presence of DNP-reactive helper T cells, and provide evidence that one critical role of helper T cell participation in humoral responses to antigens is to circumvent the development of a tolerogenic signal that, in the absence of such T cell function, might otherwise ensue after binding of the anti-genic determinants by specific B lymphocytes.
An intrastrain cross-reactive idiotype, CRIA, is associated with a large proportion of the anti-p-azophenylarsonate (anti-Ar) antibodies of A/J mice. The present experiments, in which the methods of direct and reverse passive cutaneous anaphylaxis (RPCA) were used, indicate that IgE anti-Ar antibodies are produced in A/J mice upon stimulation with a protein-Ar conjugate and that a large proportion of these antibodies express CRIA. The use of monoclonal anti-CRIA for RPCA eliminated the strong nonspecific reactions previously observed. The results provide a basis for studying factors that regulate the switch to IgE biosynthesis during an immune response.
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