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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 β receptor (LTβR) as a heterotrimeric LT
1β2 complex. LT
-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
and ltβ, but not lt
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
Abbreviations used: –/–, mice deficient in both TNFR1 and TNFR2; LT, lymphotoxin; MLN, mesenteric lymph nodes; PPs, Peyer's patches.
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