PMID- 17947706
OWN - NLM
STAT- MEDLINE
DCOM- 20071206
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 179
IP  - 9
DP  - 2007 Nov 1
TI  - Nerve growth factor promotes TLR4 signaling-induced maturation of human dendritic 
      cells in vitro through inducible p75NTR 1.
PG  - 6297-304
AB  - Nerve growth factor (NGF) has been shown to play important roles in the 
      differentiation, function, and survival of immune cells, contributing to immune 
      responses and pathogenesis of autoimmune diseases. Dendritic cells (DCs) are a 
      potent initiator for immune and inflammatory responses upon recognition of 
      pathogens via Toll-like receptors (TLR). However, expression of NGF and its 
      receptors on human monocyte-derived DCs (MoDCs) and the role of NGF in the 
      response of DCs to TLR ligands remain to be investigated. In the present study, 
      we demonstrate that there were weak expressions of NGF and no expression of NGF 
      receptors p140(TrkA) and p75(NTR) on human immature MoDCs, however, the 
      expression of NGF and p75(NTR) on MoDCs could be significantly up-regulated by 
      LPS in a dose- and time-dependent manner. NGF could markedly promote LPS-induced 
      expression of HLA-DR, CD40, CD80, CD83, CD86, CCR7, secretion of IL-12p40 and 
      proinflammatory cytokines IL-1, IL-6, TNF-alpha, and the T cell-stimulating 
      capacity of MoDCs, indicating that NGF can promote LPS-induced DC maturation. The 
      promoting effect of NGF on LPS-induced MoDCs maturation could be completely 
      abolished by pretreatment of MoDCs with p75(NTR) antagonist, suggesting that 
      LPS-induced p75(NTR) mediates the effect. Furthermore, increased activation of 
      the p38MAPK and NF-kappaB pathways has been shown to be responsible for the 
      NGF-promoted DC maturation. Therefore, NGF facilitates TLR4 signaling-induced 
      maturation of human DCs through LPS-up-regulated p75(NTR) via activation of p38 
      MAPK and NF-kappaB pathways, providing another mechanism for the involvement of 
      NGF in the immune responses and pathogenesis of autoimmune diseases.
FAU - Jiang, Yingming
AU  - Jiang Y
AD  - Institute of Immunology and National Key Laboratory of Medical Immunology, Second 
      Military Medical University, Shanghai, People's Republic of China.
FAU - Chen, Guoyou
AU  - Chen G
FAU - Zhang, Yi
AU  - Zhang Y
FAU - Lu, Lin
AU  - Lu L
FAU - Liu, Shuxun
AU  - Liu S
FAU - Cao, Xuetao
AU  - Cao X
LA  - eng
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 (Cytokines)
RN  - 0 (Ligands)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (NGFR protein, human)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Cell Differentiation/*drug effects
MH  - Cytokines/metabolism
MH  - Dendritic Cells/cytology/*drug effects/*metabolism
MH  - Gene Expression Regulation
MH  - Humans
MH  - Ligands
MH  - Lipopolysaccharides/pharmacology
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - NF-kappa B/metabolism
MH  - Nerve Growth Factors/*pharmacology
MH  - Nerve Tissue Proteins/genetics/*metabolism
MH  - Phenotype
MH  - Receptors, Nerve Growth Factor/genetics/*metabolism
MH  - Signal Transduction/*drug effects
MH  - Time Factors
MH  - Toll-Like Receptor 4/*metabolism
EDAT- 2007/10/20 09:00
MHDA- 2007/12/07 09:00
CRDT- 2007/10/20 09:00
PHST- 2007/10/20 09:00 [pubmed]
PHST- 2007/12/07 09:00 [medline]
PHST- 2007/10/20 09:00 [entrez]
AID - 179/9/6297 [pii]
AID - 10.4049/jimmunol.179.9.6297 [doi]
PST - ppublish
SO  - J Immunol. 2007 Nov 1;179(9):6297-304. doi: 10.4049/jimmunol.179.9.6297.