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New short-lived strains of mice (SAM-P), which have been developed by Takeda et al. (1981), show a defective antibody response to T dependent (TD) antigen in vitro, as demonstrated in the accompanying paper (see page 419). In the present study, we investigated the cellular site of the defect, using a cell culture system. In this paper, it is demonstrated that T-helper (Th) cell activity for the antibody response to TD antigen is impaired, while other cellular immune responses, e.g. mixed leucocyte reaction, cytotoxic T-lymphocyte response, and delayed-type hypersensitivity reaction, are normal. These results suggest that the defect in T-helper subset is limited in helper function for the antibody response, and that the helper function for the cell-mediated immune responses is intact. These two functions of the T-helper subset are apparently regulated in a different manner. The SAM-P strains of mice may thus serve as an appropriate model for studying functional heterogeneity in T-helper/inducer cell subsets. [ABSTRACT FROM AUTHOR]

Neither normal CBA (H-2k) nor purified spleen T cells respond in vitro to soluble or insoluble membrane preparations or to ultraviolet-light-inactivated stimulator cells of the allogeneic DBA/2 (H-2d) strain. However, CBA spleen cells deprived of phagocytic cells show a slight proliferative response under these conditions. After being primed against mitomycin-blocked DBA/2 cells in one-way mixed lymphocyte culture, the secondary blast-derived T `memory' cells display a good secondary blast (proliferative) response to both membrane antigens and to ultraviolet-light-inactivated stimulator cells. In addition to this, the secondary T lymphocytes--in contrast to nonprimed T cells--respond by cytotoxicity when ultraviolet-light-inactivated cells are used as the second stimulant. [ABSTRACT FROM AUTHOR]

Two distinct murine B-cell differentiation factors, designated B 151 -TRY 1 and B 151-TRF2, were described originally as B151 K12 T-cell hybridoma-derived lymphokines that induce immunoglobulin (Ig) secretion by antigen-activated B cells and unstimulated B cells, respectively. In the present study, we found that a highly purified B1 51-TRF1 fraction prepared by reversed-phase high-performance liquid chromatography (RP-H PLC) also has the ability to cause a polyclonal differentiation of unstimulated B cells into IgM-secreting cells in the apparent absence of co- stimulant. The activity of the B151-TRF1 fraction but not the B151-TRF2 fraction on unstimulated B cells was markedly inhibited by addition of a monoclonal antibody (mAb) specific for the B151- TRF 1/IL-S to the culture. To determine whether 8151 -TRF 1/IL-S and 8151 -TRF2 act on distinct populations among unstimulated B cells, the responsiveness of neonatal B cells and adult B cells that had been fractionated by Percoll density gradient centrifugation was assessed. B15 l-TRFI/IL-5 predominantly acted on lower density B cells, which appeared around 3 weeks after birth in the spleen. In contrast, B151-TRF2 could activate both lower and higher density B cells almost equally and B 151 -TRF2-responsive B cells were already present by 1 week of age. Thus, these results suggest that B151-TRFI/IL-5 and B151-TRF2 act on distinct subpopulations among antigen-unprimed normal B cells to induce IgM-secreting cells. [ABSTRACT FROM AUTHOR]

The capacity of cloned murine Ia-positive BK-BI-2.6.C6 T cells to present protein antigens to antigen-reactive long-term cultured T-cell lines was investigated. Antigen recognition by T-line cells on presenting BK-BI-2.6.C6 T-accessory cells resulted in efficient production of lymphokines. While antigen-dependent T cells with transient interleukin-2 receptor (IL-2R) expression were not induced to proliferate, T cells with constitutive IL-2R expression proliferated in response to the secreted IL-2. Although antigen presentation by BK-BI-2.6.C6 T cells resulted in a slight induction of IL-2R expression on responding T cells, as measured by flow cytometry, this augmentation was much smaller than that induced by antigen-presenting spleen cells. Thus the inability of antigen-presenting T-accessory cells to stimulate proliferation of responding T cells with transient IL-2R expression appears to reflect a lack of signal(s) necessary for the induction of IL-2R up to a level critical for initiation of cell division. This test system represents an ideal model to investigate the nature of signals required, in addition to triggering of the T-cell antigen receptor, for the induction of IL-2R. [ABSTRACT FROM AUTHOR]