PMID- 14764687
OWN - NLM
STAT- MEDLINE
DCOM- 20040615
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 172
IP  - 4
DP  - 2004 Feb 15
TI  - IL-10-conditioned dendritic cells, decommissioned for recruitment of adaptive 
      immunity, elicit innate inflammatory gene products in response to danger signals.
PG  - 2201-9
AB  - Dendritic cells (DCs) are the professional APCs of the immune system, enabling T 
      cells to perceive and respond appropriately to potentially dangerous microbes, 
      while also being able to maintain T cell tolerance toward self. In part, such 
      tolerance can be determined by IL-10 released from certain types of regulatory T 
      cells. IL-10 has previously been shown to render DCs unable to activate T cells 
      and it has been assumed that this process represents a general block in 
      maturation. Using serial analysis of gene expression, we show that IL-10 
      pretreatment of murine bone marrow-derived DCs alone causes significant changes 
      in gene expression. Furthermore, these cells retain the ability to respond to 
      Toll-like receptor agonists, but in a manner skewed toward the selective 
      induction of mediators known to enhance local inflammation and innate immunity, 
      among which we highlight a novel CXCR2 ligand, DC inflammatory protein-1. These 
      data suggest that, while the presence of a protolerogenic and purportedly 
      anti-inflammatory agent such as IL-10 precludes DCs from acquiring their 
      potential as initiators of adaptive immunity, their ability to act as initiators 
      of innate immunity in response to Toll-like receptor signaling is enhanced.
FAU - Nolan, Kathleen F
AU  - Nolan KF
AD  - Sir William Dunn School of Pathology, Oxford University, Oxford, United Kingdom. 
      kathleen.nolan@path.ox.ac.uk
FAU - Strong, Victoria
AU  - Strong V
FAU - Soler, Dulce
AU  - Soler D
FAU - Fairchild, Paul J
AU  - Fairchild PJ
FAU - Cobbold, Stephen P
AU  - Cobbold SP
FAU - Croxton, Ruth
AU  - Croxton R
FAU - Gonzalo, Jose-Angel
AU  - Gonzalo JA
FAU - Rubio, Ana
AU  - Rubio A
FAU - Wells, Meghan
AU  - Wells M
FAU - Waldmann, Herman
AU  - Waldmann H
LA  - eng
SI  - GENBANK/AY311403
SI  - GENBANK/AY311405
SI  - RefSeq/XM_284097
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 (Chemokines, CXC)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Interleukin-8B)
RN  - 0 (Tgtp protein, mouse)
RN  - 130068-27-8 (Interleukin-10)
RN  - EC 3.6.5.2 (Monomeric GTP-Binding Proteins)
SB  - IM
MH  - Amino Acid Motifs
MH  - Animals
MH  - Bone Marrow Cells/immunology/metabolism
MH  - Cell Differentiation/genetics/immunology
MH  - Cell Line
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics/*immunology
MH  - Cells, Cultured
MH  - Chemokines, CXC/antagonists & inhibitors/biosynthesis/genetics/physiology
MH  - Chemotaxis, Leukocyte/immunology
MH  - Dendritic Cells/cytology/*immunology/*metabolism
MH  - Gene Expression Regulation/*immunology
MH  - Gene Library
MH  - Humans
MH  - Immunity, Innate/genetics
MH  - Inflammation Mediators/*metabolism
MH  - Interleukin-10/*physiology
MH  - Lipopolysaccharides/pharmacology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred CBA
MH  - Molecular Sequence Data
MH  - Monomeric GTP-Binding Proteins/antagonists & 
      inhibitors/*biosynthesis/*genetics/physiology
MH  - Neutrophil Infiltration/immunology
MH  - Nucleic Acid Amplification Techniques
MH  - RNA, Messenger/biosynthesis
MH  - Receptors, Interleukin-8B/physiology
EDAT- 2004/02/07 05:00
MHDA- 2004/06/16 05:00
CRDT- 2004/02/07 05:00
PHST- 2004/02/07 05:00 [pubmed]
PHST- 2004/06/16 05:00 [medline]
PHST- 2004/02/07 05:00 [entrez]
AID - 10.4049/jimmunol.172.4.2201 [doi]
PST - ppublish
SO  - J Immunol. 2004 Feb 15;172(4):2201-9. doi: 10.4049/jimmunol.172.4.2201.