Neither lymphotoxin α nor lymphotoxin β receptor expression is required for biogenesis of lymphoid aggregates or differentiation of natural killer cells in the pregnant mouse uterus
Article first published online: 25 FEB 2003
Volume 108, Issue 3, pages 338–345, March 2003
How to Cite
Kather, A., Chantakru, S., He, H., Minhas, K., Foster, R., Markert, U. R., Pfeffer, K. and Croy, B. A. (2003), Neither lymphotoxin α nor lymphotoxin β receptor expression is required for biogenesis of lymphoid aggregates or differentiation of natural killer cells in the pregnant mouse uterus. Immunology, 108: 338–345. doi: 10.1046/j.1365-2567.2003.01586.x
- Issue published online: 25 FEB 2003
- Article first published online: 25 FEB 2003
- Received 6 March 2002; revised 27 May 2002; accepted 18 November 2002.
Gene ablation studies in mice indicate that lymphotoxin (LT)α, LTβ and LTβR are essential for the genesis of lymph nodes (LN), normal structural development of peripheral lymphoid tissues and the differentiation of natural killer (NK) cells. LTβR binds to the heterotrimeric cytokines LTα1β2 and LIGHT. LTs also regulate stromal cell expression of lymphocyte homing chemokines. Uterine decidualization in normal (+/+) mice is accompanied by the appearance and maturation of large numbers of uterine NK (uNK) cells that differentiate from precursors mobilized to the uterus from secondary lymphoid tissues. uNK cells accumulate in a transient, lymphocyte-rich region known as the metrial gland or, more recently, the mesometrial lymphoid aggregrate of pregnancy (MLAp). To determine if LTs contribute to development of the MLAp, and to the differentiation and/or localization of uNK cells, a histological study was undertaken of implantation sites from LTα null, LTβR null and gestation day-matched, normal mice. Implantation sites from the gene-ablated mice contained abundant numbers of uNK cells that localized appropriately. This indicates that the stromally derived molecules supporting NK cell differentiation in the uterus differ from those used in secondary lymphoid organs.