PMID- 17641016
OWN - NLM
STAT- MEDLINE
DCOM- 20070917
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 179
IP  - 3
DP  - 2007 Aug 1
TI  - Immunomodulatory dendritic cells inhibit Th1 responses and arthritis via 
      different mechanisms.
PG  - 1506-15
AB  - Dendritic cells (DCs) are professional APCs which have the unique ability to 
      present both foreign and self-Ags to T cells and steer the outcome of immune 
      responses. Because of these characteristics, DCs are attractive vehicles for the 
      delivery of therapeutic vaccines. Fully matured DCs are relatively well-defined 
      and even used in clinical trials in cancer. DCs also have the potential to 
      influence the outcome of autoimmunity by modulating the underlying autoimmune 
      response. To gain a better appreciation of the abilities and mechanisms by which 
      immunomodulatory DCs influence the outcome of T cell responses, we studied 
      several immunomodulatory DCs (TNF-, IL-10-, or dexamethasone-stimulated bone 
      marrow-derived DCs) side by side for their ability to modulate T cell responses 
      and autoimmune diseases. Our data show that these differentially modulated DCs 
      display a different composition of molecules involved in T cell activation. 
      Although, all DC subsets analyzed were able to inhibit the induction of 
      collagen-induced arthritis, the modulation of the underlying immune response was 
      different. Vaccination with TNF- or IL-10-modulated DCs altered the Th1/Th2 
      balance as evidenced by the induction of IL-5- and IL-10-secreting T cells and 
      the concomitant reduction of the IgG2a-IgG1 ratio against the immunizing Ag. In 
      contrast, DCs modulated with dexamethasone did not affect the ratio of 
      IL-5-producing vs IFN-gamma-producing T cells and tended to affect the Ab 
      response in a nonspecific manner. These data indicate that distinct mechanisms 
      can be used by distinct DC subsets to change the outcome of autoimmunity.
FAU - van Duivenvoorde, Leonie M
AU  - van Duivenvoorde LM
AD  - Department of Rheumatology, Leiden University Medical Center, Leiden, The 
      Netherlands.
FAU - Han, Wanda G H
AU  - Han WG
FAU - Bakker, Aleida M
AU  - Bakker AM
FAU - Louis-Plence, Pascale
AU  - Louis-Plence P
FAU - Charbonnier, Louis-Marie
AU  - Charbonnier LM
FAU - Apparailly, Florence
AU  - Apparailly F
FAU - van der Voort, Ellen I H
AU  - van der Voort EI
FAU - Jorgensen, Christian
AU  - Jorgensen C
FAU - Huizinga, Tom W J
AU  - Huizinga TW
FAU - Toes, Rene E M
AU  - Toes RE
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Collagen Type II)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Arthritis, Experimental/*immunology/*prevention & control
MH  - Cells, Cultured
MH  - Collagen Type II/administration & dosage/immunology
MH  - Dendritic Cells/drug effects/*immunology/*transplantation
MH  - Dexamethasone/pharmacology
MH  - *Immune Tolerance/drug effects
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred DBA
MH  - Mice, Transgenic
MH  - Th1 Cells/*immunology/metabolism
EDAT- 2007/07/21 09:00
MHDA- 2007/09/18 09:00
CRDT- 2007/07/21 09:00
PHST- 2007/07/21 09:00 [pubmed]
PHST- 2007/09/18 09:00 [medline]
PHST- 2007/07/21 09:00 [entrez]
AID - 179/3/1506 [pii]
AID - 10.4049/jimmunol.179.3.1506 [doi]
PST - ppublish
SO  - J Immunol. 2007 Aug 1;179(3):1506-15. doi: 10.4049/jimmunol.179.3.1506.