Inactivation of genes encoding members of TNF and TNF receptor families reveal their divergent roles in the formation and function of secondary lymphoid organs. Most lymphotoxin α (ltα)- and all lymphotoxin β receptor (ltβr)-deficient mice are completely devoid of lymph nodes (LNs); however, most lymphotoxin β (ltβ)-deficient mice develop mesenteric LNs. Tnf- and tnfrp55-deficient mice develop a complete set of LNs, while ltβ/tnfrp55 double-deficient mice lack all LNs, demonstrating cooperation between LTβ and TNFRp55 in LN development. Now we report that ltβ/tnf double-deficient mice develop the same set of mucosal LNs as do ltβ-deficient mice, suggesting that ligands other than TNF signal through TNFRp55 during LN development. These LNs retain distinct T and B cells areas; however, they lack follicular dendritic cell networks. Structures resembling germinal centers can be found in the LNs from immunized ltβ-deficient mice but not in ltβ/tnf double-deficient mice. Additionally, stromal components of the spleen and LNs appear to be more severely disturbed in ltβ/tnf double- deficient mice as compared with ltβ-deficient mice. We conclude that LTβ and TNF cooperate in the establishment of the correct microarchitecture of lymphoid organs.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Immunology|
|State||Published - Dec 28 1999|
ASJC Scopus subject areas
- Immunology and Allergy