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B (RANK)/RANK Ligand Interactions: Impact on Tolerance Induction
Department of Inflammation, Immunex Corp., Seattle WA 98101
The mucosal immune system is uniquely equipped to discriminate
between potentially invasive pathogens and innocuous food proteins.
While the mechanisms responsible for induction of mucosal immunity vs
tolerance are not yet fully delineated, recent studies have highlighted
mucosal dendritic cells (DC) as being important in determining the fate
of orally administered Ag. To further investigate the DC:T cell signals
involved in regulating the homeostatic balance between mucosal immunity
and tolerance, we have examined the expression and function of the TNFR
family member receptor activator of NF-
B (RANK) and its cognate
ligand, RANKL, in vitro and in vivo. Our data show that although DC
isolated from mucosal lymphoid tissues expressed similar levels of
surface RANK compared with DC isolated from peripheral lymphoid
tissues, DC from the distinct anatomical sites displayed differential
responsiveness to RANK engagement with soluble RANKL. Whereas splenic
DC responded to RANKL stimulation with elevated IL-12 p40 mRNA
expression, Peyer’s patch DC instead preferentially displayed
increased IL-10 mRNA expression. Our data also show that the in vivo
functional capacity of mucosal DC can be modulated by RANKL. Treatment
with RANKL in vivo at the time of oral administration of soluble OVA
enhanced the induction of tolerance in two different mouse
models. These studies underscore the functional differences
between mucosal and peripheral DC and highlight a novel role for
RANK/RANKL interactions during the induction of mucosal immune
responses.
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