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Antibody against T cell-replacing factor acceptor site(s) augments in vivo primary IgM responses to suboptimal doses of heterologous erythrocytes

Abstract

It is widely accepted that B cells possess two distinct receptors. One is the surface immunoglobiilin that recognizes the antigenic determinant; the other transmits the signals for proliferation and differentiation of the B cells after receiving differentiation stimuli mediated by a soluble factor derived from helper T cells. Previously1–4, we demonstrated that the responsivity of B cells to T cell-replacing factor (TRF) was under X-chromosome control, as determined by genetic analysis of the TRF-nonres-ponsiveness of B cells from DBA/ 2Ha mice. An X-linked B-cell defect of DBA/2Ha mice to TRF seemed to be due to the absence of an acceptor site(s). We have immunized the defective (DBA/2Ha♀×BALB/c♂)F1 male mice with antigen-primed parental BALB/c splenic B cells. The resulting alloantiserum preferentially inhibited the B-cell response mediated in vitro by TRF added continuously to the culture. We report here that this antiserum, which presumably contains antibody against the putative TRF-acceptor site, augments primary IgM responses to simultaneously administered suboptimal doses of heterologous erythrocytes injected into TRF high-responder animals. These augmented IgM-PFC (plaque -forming cell) responses were also observed in other X-Iinked B-cell defective CBA/N mice, but not in TRF low-responder DB A/2Ha mice, suggesting that the putative TRF-acceptor site(s) functionally detectable by this antiserum is distinct from the Lyb 3 and Lyb 5 components.

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Takatsu, K., Sano, Y., Tomita, S. et al. Antibody against T cell-replacing factor acceptor site(s) augments in vivo primary IgM responses to suboptimal doses of heterologous erythrocytes. Nature 292, 360–362 (1981). https://doi.org/10.1038/292360a0

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