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3 and Membrane Lymphotoxin-1ß2 in Lymphotoxin-Induced Inflammation: Critical Role of TNF Receptor 1 Signaling1
*
Department of Epidemiology and Public Health and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; and
Department of Nervous System Diseases PRPN, F. Hoffmann-La Roche, Basel, Switzerland
Lymphotoxin (LT, LT
, TNFß) is a member of the immediate TNF
family that also includes TNF- and lymphotoxin-ß (LTß). LT is
produced by activated lymphocytes and functions as either a secreted
homotrimer or a membrane-associated heterotrimer that includes the
transmembrane protein LTß. Secreted LT3 can bind
to two cell surface receptors, TNFR1 and TNFR2, while the
membrane-bound heterotrimer LT1ß2 has been
shown to interact with a distinct receptor, LTßR. LT induces
inflammation at the sites of expression of a rat insulin
promoter-driven lymphotoxin (RIPLT) transgene in the pancreas and
kidney. To determine the role of the various ligands and their
receptors in LT-induced inflammation, mice deficient in either TNFR1,
TNFR2, or LTß were crossed to RIPLT-transgenic mice. Our results
indicate that LT-induced inflammation is dependent on the
interaction of LT3 with TNFR1, and there is no obvious
role for TNFR2, since in its absence, LT-induced inflammation is
quantitatively and qualitatively similar to that seen in the wild type.
However, the absence of LTß results in accentuated infiltration of
the kidney with an increase in the proportion of memory cells in the
infiltrate. These data show a crucial role for the secreted
LT3 signaling via TNFR1 in LT-induced inflammation,
and a separate and distinct role for the membrane
LT1ß2 form in this inflammatory process.
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