PMID- 16621985
OWN - NLM
STAT- MEDLINE
DCOM- 20060606
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 176
IP  - 9
DP  - 2006 May 1
TI  - Regulation of intestinal dendritic cell migration and activation by plasmacytoid 
      dendritic cells, TNF-alpha and type 1 IFNs after feeding a TLR7/8 ligand.
PG  - 5205-12
AB  - Dendritic cells (DCs) migrating via lymph are the primary influence regulating 
      naive T cell differentiation, be it active immunity or tolerance. How DCs achieve 
      this regulation in vivo is poorly understood. Intestinal DCs are in direct 
      contact with harmless or pathogenic luminal contents, but may also be influenced 
      by signals from epithelial cells, macrophages, or other resident or immigrant 
      cells. To understand the role of TLR7 and TLR8 in regulating intestinal DC 
      function, we fed a TLR7/8 ligand (resiquimod (R-848)) to rats and mice and 
      examined DC in pseudoafferent lymph (rat) and mesenteric lymph nodes (MLNs). Oral 
      R-848 induced a 20- to 30-fold increase in DC output from the intestine within 10 
      h due to a virtually total release of lamina propria DCs. This resulted in an 
      accumulation of DCs in the MLNs that in mice was completely TNF-alpha dependent. 
      Surprisingly, intestinal lymph DCs (iL-DCs) released by R-848 did not up-regulate 
      CD86, but did up-regulate CD25. In contrast, MLN-DCs from R-848-stimulated rats 
      and mice expressed high levels of CD86. This DC activation in MLNs was dependent 
      on type 1 IFNs. The major source of these rapidly released cytokines is 
      plasmacytoid DCs (pDCs) and not classical DCs, because depletion of pDCs 
      significantly reduces the R-848-stimulated increase in serum cytokine levels as 
      well as the accumulation and activation of DCs in MLNs. These experiments show 
      that TLR-mediated regulation of iL-DC functions in vivo is complex and does not 
      depend only on direct iL-DC stimulation, but can be regulated by pDCs.
FAU - Yrlid, Ulf
AU  - Yrlid U
AD  - Sir William Dunn School of Pathology, South Parks Road, Oxford, United Kingdom.
FAU - Milling, Simon W F
AU  - Milling SW
FAU - Miller, Joanna L
AU  - Miller JL
FAU - Cartland, Sian
AU  - Cartland S
FAU - Jenkins, Christopher D
AU  - Jenkins CD
FAU - MacPherson, G Gordon
AU  - MacPherson GG
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Imidazoles)
RN  - 0 (Interferon Type I)
RN  - 0 (Ligands)
RN  - 0 (Toll-Like Receptor 7)
RN  - 0 (Toll-Like Receptor 8)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - V3DMU7PVXF (resiquimod)
SB  - IM
MH  - Animal Feed
MH  - Animals
MH  - Cell Movement/immunology
MH  - Cells, Cultured
MH  - Dendritic Cells/*cytology/*immunology/metabolism
MH  - Imidazoles/pharmacology
MH  - Interferon Type I/genetics/immunology/*metabolism
MH  - Intestinal Mucosa/metabolism
MH  - Intestines/cytology/*immunology
MH  - Ligands
MH  - Mice
MH  - Mice, Knockout
MH  - Plasma Cells/cytology/immunology/metabolism
MH  - Rats
MH  - Toll-Like Receptor 7/*immunology
MH  - Toll-Like Receptor 8/*immunology
MH  - Tumor Necrosis Factor-alpha/immunology/*metabolism
EDAT- 2006/04/20 09:00
MHDA- 2006/06/07 09:00
CRDT- 2006/04/20 09:00
PHST- 2006/04/20 09:00 [pubmed]
PHST- 2006/06/07 09:00 [medline]
PHST- 2006/04/20 09:00 [entrez]
AID - 176/9/5205 [pii]
AID - 10.4049/jimmunol.176.9.5205 [doi]
PST - ppublish
SO  - J Immunol. 2006 May 1;176(9):5205-12. doi: 10.4049/jimmunol.176.9.5205.