INVESTIGADORES
VERMEULEN Elba Monica
artículos
Título:
Impaired function of dendritic cells deficient in angiotensin II type 1 receptors.
Autor/es:
NAHMOD K; GENTILINI C; VERMEULEN M; UHAREK L; WANG Y; ZHANG J; SCHULTHEISS HP; GEFFNER J; WALTHER T
Revista:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Editorial:
AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
Referencias:
Año: 2010 vol. 334 p. 854 - 862
ISSN:
0022-3565
Resumen:
Dendritic cells (DC) are highly specialized antigen-presenting
cells with a unique ability to activate resting T lymphocytes and
initiate primary immune responses. Angiotensin II (AII) is involved
in key events of the inflammatory response. Because
our previous work implicated an effect of AII on differentiation
and function of murine and human DC, we investigated the
impact of AII type 1 receptor (AT1) deficiency on the phenotypical
and functional properties of mouse DC in vitro and in vivo.
Bone marrow (BM) cells isolated from mice lacking AII subtype
1a receptor (AT1a), AII subtype 1b receptor (AT1b), or both
receptor isoforms and control littermates [wild type (WT)] were
cultured for 7 days in the presence of recombinant mouse
granulocyte/macrophage colony-stimulating factor to generate
myeloid DC in vitro. Generation of CD11c cells was less
efficient in both AT1a- and AT1b-deficient BM cells than in WT
BM cell cultures. Moreover, DC generated from AT1-deficient
progenitors showed lower levels of expression of major histocompatibility
complex II (MHC-II) and CD11c (p 0.01) and a
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
progenitors showed lower levels of expression of major histocompatibility
complex II (MHC-II) and CD11c (p 0.01) and a
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
BM cell cultures. Moreover, DC generated from AT1-deficient
progenitors showed lower levels of expression of major histocompatibility
complex II (MHC-II) and CD11c (p 0.01) and a
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
progenitors showed lower levels of expression of major histocompatibility
complex II (MHC-II) and CD11c (p 0.01) and a
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
efficient in both AT1a- and AT1b-deficient BM cells than in WT
BM cell cultures. Moreover, DC generated from AT1-deficient
progenitors showed lower levels of expression of major histocompatibility
complex II (MHC-II) and CD11c (p 0.01) and a
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
progenitors showed lower levels of expression of major histocompatibility
complex II (MHC-II) and CD11c (p 0.01) and a
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
BM cell cultures. Moreover, DC generated from AT1-deficient
progenitors showed lower levels of expression of major histocompatibility
complex II (MHC-II) and CD11c (p 0.01) and a
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
progenitors showed lower levels of expression of major histocompatibility
complex II (MHC-II) and CD11c (p 0.01) and a
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
marked reduction in their allostimulatory activity (p 0.01 or
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
0.001). Although AT1-deficient DC released comparable levels
of interleukin (IL)-10 and IL-12p70 to WT DC, they produced
significantly lower levels of tumor necrosis factor (TNF-) (p
of interleukin (IL)-10 and IL-12p70 to WT