J. Exp. Med., Volume 187, Number 12, June 15, 1998 1977-1983

A Role for Tumor Necrosis Factor Receptor Type 1 in Gut-associated Lymphoid Tissue Development: Genetic Evidence of Synergism with Lymphotoxin  

By Pandelakis A. Koni^* and Richard A. Flavell^*

From the ^* Section of Immunobiology and the  Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520

Lymphotoxin  (LT) signals via tumor necrosis factor receptors (TNFRs) as a homotrimer and via lymphotoxin  receptor (LTR) as a heterotrimeric LT₁₂ complex. LT-deficient mice lack all lymph nodes (LNs) and Peyer's patches (PPs), and yet LT-deficient mice and TNFR-deficient mice have cervical and mesenteric LN. We now show that mice made deficient in both LT and TNFR type 1 (TNFR1) lack all LNs, revealing redundancy or synergism between TNFR1 and LT, acting presumably via LTR. A complete lack of only PPs in mice heterozygous for both lt and lt, but not lt or lt alone, suggests a similar two-ligand phenomenon in PP development and may explain the incomplete lack of PPs seen in tnfr1^/ mice.

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