Unresponsiveness of MRL/MP-lpr/lpr mice to antigen given subcutaneously in adjuvant: partial restoration of response after local injection of B cells.

MRL/lpr mice were used as a model for seeking information on the role of B cells as antigen-presenting cells in vivo. In confirmation of the finding of other workers, MRL/lpr mice with pronounced lymphadenopathy failed to undergo T cell priming in lymph nodes (LN) after s.c. injection of keyhole limpet hemocyanin (KLH) in complete Freund's adjuvant (CFA): thus, in contrast to normal mice or young MRL/lpr mice, the LN cells from older MRL/lpr mice failed to give secondary T proliferative responses to the injected antigen in vitro. Because previous work from this laboratory has shown that B cells play a major role in priming T cells in LN of normal mice, we tested the possibility that the lack of T cell priming to KLH seen in older MRL/lpr LN reflected the relative paucity of B cells. To test this idea, MRL/LPR mice were injected s.c. with B cells taken from normal or young MRL/lpr mice 1 day before priming with KLH/CFA. In the case of old (20 to 24 wk) MRL/lpr mice with massive lymphadenopathy, prior injection of B cells had virtually no effect in promoting LN priming. In marked contrast, injection of B cells into mice exhibiting less-pronounced LN enlargement (mice tested at 14 to 16 wk) was highly effective in restoring LN priming; before B cell injection, the LN of these mice contained only 2 to 5% B cells. These findings add to the evidence that T cell priming in LN is heavily dependent on the presence of B cells.