Description
Loss of the interactions between lymphotoxin and its receptor was associated with MZM apoptotic cell clearance defects in BXD2 mice whereas loss of IFNAR in BXD2 mice normalized the function of MZMs. The analysis also intended to use MZMs isolated from BXD2-Ifnar-/- mice and BXD2 mice treated with sLTbR-Fc to identify the common pathways regulating the MZM function in these mice.