“…However, the secondary lymphoid organ phenotype of our NIK KO/KO mice appears to recapitulate the phenotype observed in NF-kB2-deficient mice (17,46) and is also very similar to that observed in LTb-deficient mice (26,47,48). Deficiency of NIK and various NF-kB family members that mediate noncanonical NF-kB signaling leads to similar, but not completely identical, secondary lymphoid organ defects (55), and secondary lymphoid organ development is exquisitely sensitive to slight differences in lymphotoxin/LTbR signaling, as revealed by studies of mice deficient in NIK and various NF-kB family members, studies of mice deficient in the lymphotoxin subunits LTa and LTb and the lymphotoxin receptor LTbR (17,56,57), and studies of temporal blockade of LTbR signaling at different times in utero (24,58,59). Thus, the differences in secondary lymphoid organ phenotypes between our NIK KO/KO mice and NIK aly/aly mice, as well as the other NIK-deficient mouse strain, may arise from Upon acute deletion of NIK in adult mice using our conditional NIK KO allele, we observed the abrogation of noncanonical NF-kB signaling, as assessed by p52 production, and a resulting reduction in B cell numbers in lymph nodes and spleen.…”