@Article{ecn.2008.0121,
AUTHOR = {Sara Scutera, Elena Riboldi, Roberta Daniele, Angela Rita Elia, Tiziana Fraone, Carlotta Castagnoli, Mirella Giovarelli, Tiziana Musso, Silvano Sozzani},
TITLE = {Production and function of activin A in human dendritic cells},
JOURNAL = {European Cytokine Network},
VOLUME = {19},
YEAR = {2008},
NUMBER = {1},
PAGES = {60--68},
URL = {http://www.techscience.com/ECN/v19n1/65949},
ISSN = {1952-4005},
ABSTRACT = {Activin A, a member of the transforming growth factor-b superfamily, has a role in tissue repair and
inflammation. In our previous studies, we identified by immunohistochemistry DC-SIGN(+) dendritic cells as a
source of activin A in vivo. The present study was aimed at investigating activin A production by dendritic cells
(DC) in vitro and its function. Here we demonstrate that monocyte-derived DC (Mo-DC) released abundant levels
of activin A during the maturation process induced by TLR agonists, bacteria (<i>B. henselae</i>, <i>S. thyphimurium</i>), TNF
and CD40L. Activin A was also induced in monocyte-derived Langerhans cells (LC) and in blood myeloid DC by
LPS and/or CD40L stimulation, but not in blood plasmacytoid DC following stimulation with influenza virus.
Activin A production by DC was selectively down-regulated by anti-inflammatory molecules such as dexametha-sone
or IL-10. Neutralization of endogenous activin A using its inhibitor follistatin, or the addition of exogenous
activin A during LPS maturation did not affect Mo-DC maturation marker expression, cytokine release or
allostimulatory function. However, Mo-DC matured with LPS in the presence of exogenous activin A displayed a
higher FITC-dextran uptake, similar to that of immature DC. Moreover, activin A promoted monocyte
differentiation to DC and reversed the inhibitory effects of IL-6 on DC differentiation of monocytes. These findings
demonstrate that different subsets of DC release activin A, a cytokine that promotes DC generation, and affects
the ability of mature DC to take up antigens (Ags).},
DOI = {10.1684/ecn.2008.0121}
}