The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/6/1977/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 12, June 15, 1998 1977-1983

Articles

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

Pandelakis A. Koni* and Richard A. Flavell*,{ddagger}

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

Lymphotoxin {alpha} (LT{alpha}) signals via tumor necrosis factor receptors (TNFRs) as a homotrimer and via lymphotoxin β receptor (LTβR) as a heterotrimeric LT{alpha}1β2 complex. LT{alpha}-deficient mice lack all lymph nodes (LNs) and Peyer's patches (PPs), and yet LTβ-deficient mice and TNFR-deficient mice have cervical and mesenteric LN. We now show that mice made deficient in both LTβ and TNFR type 1 (TNFR1) lack all LNs, revealing redundancy or synergism between TNFR1 and LTβ, acting presumably via LTβR. A complete lack of only PPs in mice heterozygous for both lt{alpha} and ltβ, but not lt{alpha} or ltβ alone, suggests a similar two-ligand phenomenon in PP development and may explain the incomplete lack of PPs seen in tnfr1–/– mice.

Key Words: lymphotoxin beta • tumor necrosis factor receptor 1 • knockout mice • mesenteric lymph nodes • Peyer's patches

Address correspondence to R.A. Flavell, Section of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, 310 Cedar Street, FMB 412, New Haven, CT 06520. Phone: 203-737-2216; Fax: 203-785-7561; E-mail: richard.flavell{at}qm.yale.edu

Abbreviations used: –/–, mice deficient in both TNFR1 and TNFR2; LT, lymphotoxin; MLN, mesenteric lymph nodes; PPs, Peyer's patches.


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