@misc{10481/99338,
year = {2006},
url = {https://hdl.handle.net/10481/99338},
abstract = {The generation of pathogen-specific immune
responses is dependent on the signaling
capabilities of pathogen-recognition
receptors. DC-SIGN is a C-type lectin that
mediates capture and internalization of viral,
bacterial, and fungal pathogens by myeloid
dendritic cells. DC-SIGN–interacting
pathogens are thought to modulate dendritic
cell maturation by interfering with intracellular
signaling from Toll-like receptor molecules.
We report that engagement of DCSIGN
by specific antibodies does not
promote dendritic cell maturation but induces
ERK1/2 and Akt phosphorylation
without concomitant p38MAPK activation.
DC-SIGN ligation also triggers PLC 
phosphorylation and transient increases
in intracellular calcium in dendritic cells.
In agreement with its signaling capabilities,
a fraction of DC-SIGN molecules
partitions within lipid raft–enriched membrane
fractions both in DC-SIGN–transfected
and dendritic cells. Moreover, DCSIGN
in dendritic cells coprecipitates with
the tyrosine kinases Lyn and Syk. The
relevance of the DC-SIGN–initiated signals
was demonstrated in monocytederived
dendritic cells, as DC-SIGN crosslinking
synergizes with TNF-  for IL-10
release and enhances the production of
LPS-induced IL-10. These results demonstrate
that DC-SIGN–triggered intracellular
signals modulate dendritic cell maturation.
Since pathogens stimulate Th2
responses via preferential activation of
ERK1/2, these results provide a molecular
explanation for the ability of DC-SIGN–
interacting pathogens to preferentially
evoke Th2-type immune responses.},
title = {DC-SIGN ligation on dendritic cells results in ERK and PI3K activation and modulates cytokine production},
author = {Muñoz Fernández, Pilar and Caparrós, Esther and Sierra Filardi, E. and Serrano Gómez, Diego and Puig-Kröger, A. and Rodríguez Fernández, J.L. and Mellado, M. and Sancho, Jaime and Zubiaur, Mercedes and Corbí, A},
}