Genetic analysis of the B cell responsiveness to T cell-replacing factor (TRF) was carried out employing an in vitro secondary anti-DNP antibody response. B cells from DBA/2Ha mice were low responders to the BALB/ c-TRF, although the TRF exerted its activity on other entirely allogeneic B cells beyond the major histocompatibility barrier. By taking advantage of the low-response character of DBA/2Ha B cells to BALB/c-TRF, the functional property of TRF responsiveness was genetically analyzed with B cells from an F1 hybrid between the low-re-sponder strain DBA/2Ha (♀) and high responder strain BALB/c (♂) or reciprocal F1 hybrids. The B cells from all male mice (DBA/2Ha X BALB/c) (DC) F1 tested were incapable of responding to TRF, whereas B cells from female mice of the same litter as the DCF1 as well as both male and female (BALB/c X DBA/2Ha) (CD) F1 mice responded to TRF. These results suggested that the responsivity of B cells to TRF was linked to the X chromosome of the high-response animals. The absence or low expression of TRF-acceptor site(s) on B cells of the low-responder strain DBA/2Ha was indicated by the failure in absorbing TRF activity. Moreover, the alloantisera raised in the low-responder DCF1 male mice by immunization with high-responder parental BALB/c B cells invariably inhibited the in vitro B cell reponse mediated by TRF when added continuously to the culture. However, these alloantisera did not inhibit cognate T-B cell interactions, suggesting that the above antisera may specifically block TRF-acceptor site(s) on B cells. Moreover, the fact that the antiserum activity was absorbed with BALB/c and C57BL/10 (high-responder strains) spleen cells but not with DBA/2Ha cells further indicated the absence of TRF-acceptor sites on DBA/2Ha B cells.
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Tominaga et al. (1980) studied this question.