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4ß1 Integrin, Peripheral Node Addressin/L-Selectin, and Lymphocyte Function-Associated Antigen-1 Adhesion Pathways
From the Department of Pathology,*
Stanford
University School of Medicine, Stanford, California; the Pathology and
Laboratory Medicine Service,
Department of
Veterans Affairs, Palo Alto Health Care System, Palo Alto, California;
and the Department of Environmental Medicine,
Kagoshima University Faculty of Medicine, Kagoshima, Japan
Sjogren’s syndrome is an autoimmune disease characterized by
inflammation and destruction of lacrimal and salivary glands. The
development of the inflammation requires the migration of lymphocytes
from the blood into these tissues. This migration involves multistep
cascades with binding of lacrimal gland endothelial adhesion molecules
to their ligands on circulating lymphocytes. We used nonobese diabetic
mice, which develop autoimmune-mediated lacrimal gland
inflammation, as an experimental model to define the adhesion
molecules that control lymphocyte migration into inflamed lacrimal
glands. We found that vascular endothelia in inflamed areas of lacrimal
gland expressed vascular cell adhesion molecule (VCAM)-1 and the
peripheral node addressin (PNAd), but not mucosal addressin
cell adhesion molecule-1. Most lymphocytes in the inflamed glands
expressed 
4 integrin, L-selectin, and
lymphocyte function-associated antigen (LFA)-1. In vivo
studies revealed that antibodies against VCAM-1,
4 integrin, PNAd, L-selectin, or
LFA-1 almost completely blocked lymphocyte migration from blood into
inflamed lacrimal glands. There was no inhibition of migration by
antibodies against mucosal addressin cell adhesion molecule-1 or
4ß7 integrin. These results indicate that
endothelial/lymphocyte adhesion cascades involving
VCAM-1/4ß1 integrin,
PNAd/L-selectin, and LFA-1 control the migration of lymphocytes
into inflamed lacrimal gland. These adhesion molecules offer potential
therapeutic targets to block the development of lacrimal gland
inflammation and destruction.
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