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3 Induces Chemokines and Adhesion Molecules: Insight into the Role of LT in Inflammation and Lymphoid Organ Development1
*
Departments of Epidemiology and Public Health, Immunobiology, and
Internal Medicine (Cardiovascular Medicine), Yale University School of Medicine, New Haven, CT 06520; and
Department of Physiology, University of Michigan School of Medicine, Ann Arbor, MI 48109
Lymphotoxin (LT) plays an important role in inflammation
and lymphoid organ development, though the mechanisms by which it
promotes these processes are poorly understood. Toward this end, the
biologic activities of a recently generated recombinant murine (m)
LT
preparation were evaluated. This cytokine preparation was
effective at inducing cytotoxicity of WEHI target cells with 50%
maximal killing observed with 1.2 ng/ml. mLT also induced the
expression of inflammatory mediators in the murine endothelial cell
line bEnd.3. rmLT induced expression of the adhesion molecules VCAM,
ICAM, E-selectin, and the mucosal addressin cellular adhesion molecule,
MAdCAM-1. When mLT, human (h) LT, and mTNF- were compared,
mLT was the most potent inducer of MAdCAM-1. None of these cytokines
induced the peripheral node addressin, PNAd. mLT also induced
expression of the chemokines RANTES, IFN-inducible protein 10 (IP-10),
and monocyte chemotactic protein 1 (MCP-1). mRNA levels peaked 4 h
following treatment with mLT and declined through the 24-h treatment
period. LT also induced chemokine protein within 8 h of
treatment, which increased through the 24-h treatment period. These
data demonstrate that the proinflammatory effects of LT3 may be
mediated in part through the induction of adhesion molecule and
chemokine expression. Further, LT3 may promote development of
lymphoid tissue through induction of chemokines and the mucosal
addressin MAdCAM-1. These data confirm previous observations in
transgenic and knockout mice that LT3 in the absence of LTß
carries out unique biologic activities.
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