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and the Lymphotoxin 
Receptor1
* Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322;
Department of Medicine B, University of Münster, Münster, Germany; and
Department of Surgery, Emory University School of Medicine, Atlanta, GA 30322
Interactions between lymphotoxin (LT)
1
2 on inducer cells and the lymphotoxin receptor (LTR) on stromal cells initiate development of lymph nodes and Peyer’s patches. In this study, we assessed the contributions of LT and LTR to the development of cryptopatches (CP), aggregates of T cell precursors in the mouse small intestine. Mice genetically deficient in LT or LTR lacked CP. Bone marrow from LT-deficient mice was unable to initiate development of CP or isolated lymphoid follicles (ILF) after transfer to CD132-null mice lacking CP and ILF. However, LT-deficient bone marrow-derived cells contributed to CP formed in CD132-null mice receiving a mixture of wild-type and LT-deficient bone marrow cells. Transfer of wild-type bone marrow into irradiated LT-deficient mice resulted in reconstitution of both CP and ILF. However, the LT-dependent formation of CP was distinguished from the LT-dependent formation of ILF and Peyer’s patches by not requiring the presence of an intact NF-
B-inducing kinase gene. CP but not ILF were present in the small intestine from NF-B-inducing kinase-deficient alymphoplasia mice, indicating that the alternate NF-B activation pathway required for other types of LTR-dependent lymphoid organogenesis is dispensable for CP development. In addition, we identified VCAM-1+ cells within both CP and ILF that are candidates for the stromal cells involved in receiving LT-dependent signals from the hemopoietic precursors recruited to CP. These findings demonstrate that interactions between cells expressing LT12 and LTR are a shared feature in the development of all small intestinal lymphoid aggregates.
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