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3 and LTß in Inflammation Elucidates Potential Mechanisms of Mesenteric and Peripheral Lymph Node Development1
Department of Epidemiology and Public Health and Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520
Lymphotoxin (LT) is a member of the proinflammatory TNF family of
cytokines that plays a critical role in the development of lymphoid
tissue. It has previously been reported that the presence of the LT
transgene under the control of the rat insulin promoter results in
inflammation at the sites of transgene expression. LT transgene
expression results in expression of the adhesion molecules VCAM, ICAM,
peripheral node addressin (a marker of peripheral lymph nodes), and
mucosal addressin cellular adhesion molecule (a marker of mucosal
lymphoid tissue, including mesenteric lymph nodes). In this study to
determine the mechanisms by which LT promotes inflammation and lymphoid
tissue organization, we analyzed the regulation of expression of
adhesion molecules and chemokines in LT transgenic mice. The results
demonstrate that LT3 induces expression of the adhesion molecules
VCAM, ICAM, and mucosal addressin cellular adhesion molecule as well as
the chemokines RANTES, IFN-inducible protein-10, and monocyte
chemotactic protein-1, while LTß is required for the induction of
peripheral node addressin that may contribute to the recruitment of
L-selectinhigh CD44low naive T cells. These
data provide candidate mediators of LT-induced inflammation as well as
potential mechanisms by which LT and LTß may differentially
promote the development of mesenteric and peripheral lymph
nodes.
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