PMID- 14632659
OWN - NLM
STAT- MEDLINE
DCOM- 20031215
LR  - 20201208
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 110
IP  - 3
DP  - 2003 Nov
TI  - Role of early- or late-phase activation of p38 mitogen-activated protein kinase 
      induced by tumour necrosis factor-alpha or 2,4-dinitrochlorobenzene during 
      maturation of murine dendritic cells.
PG  - 322-8
AB  - Dendritic cells (DCs) are maturated by a variety of stimuli. However, the precise 
      mechanisms underlying the maturation of DCs are not fully understood. In the 
      present study, we analysed the effects of tumour necrosis factor-alpha 
      (TNF-alpha) and 2,4-dinitrochlorobenzene (DNCB) on phenotypic maturation and p38 
      mitogen activated protein kinase (MAPK) activity, using a murine DC line. 
      TNF-alpha markedly increased the surface expression of major histocompatibility 
      complex (MHC) and costimulatory molecules, CD86 and CD80, on DCs. DNCB more 
      markedly enhanced the surface expression of costimulatory molecules, but showed 
      less stimulatory capability on MHC molecules, compared with TNF-alpha. 
      Simultaneous treatment of DCs with TNF-alpha and DNCB showed additive enhancement 
      of costimulatory molecule expression. TNF-alpha activated p38 MAPK in DCs only at 
      an early time-point (15 min). In contrast, DNCB activated p38 MAPK at later 
      time-points (3-6 hr). SB203580, a specific inhibitor of p38 MAPK, partially or 
      markedly inhibited the phenotypic changes of DCs induced by TNF-alpha or DNCB, 
      respectively. In addition, N-acetyl-l-cysteine, a reducing supplier, completely 
      inhibited the DNCB-induced expression of MHC and costimulatory molecules, but not 
      those induced by TNF-alpha. These findings demonstrate that TNF-alpha and DNCB 
      activate the p38 MAPK pathway at an early and a late phase, respectively, and 
      thereby induce DC maturation through different signal pathways.
FAU - Iijima, Norifumi
AU  - Iijima N
AD  - Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, 
      Sapporo, Japan.
FAU - Yanagawa, Yoshiki
AU  - Yanagawa Y
FAU - Onoe, Kazunori
AU  - Onoe K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Antigens, CD)
RN  - 0 (B7-1 Antigen)
RN  - 0 (B7-2 Antigen)
RN  - 0 (Cd86 protein, mouse)
RN  - 0 (Dinitrochlorobenzene)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - WYQ7N0BPYC (Acetylcysteine)
SB  - IM
MH  - Acetylcysteine/pharmacology
MH  - Animals
MH  - Antigens, CD/metabolism
MH  - B7-1 Antigen/metabolism
MH  - B7-2 Antigen
MH  - Cell Differentiation/drug effects
MH  - Cells, Cultured
MH  - Dendritic Cells/*drug effects/enzymology/immunology
MH  - Dinitrochlorobenzene/antagonists & inhibitors/*pharmacology
MH  - Drug Synergism
MH  - Immunophenotyping
MH  - Membrane Glycoproteins/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mitogen-Activated Protein Kinases/drug effects/*metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - p38 Mitogen-Activated Protein Kinases
PMC - PMC1783058
EDAT- 2003/11/25 05:00
MHDA- 2003/12/16 05:00
PMCR- 2004/11/01
CRDT- 2003/11/25 05:00
PHST- 2003/11/25 05:00 [pubmed]
PHST- 2003/12/16 05:00 [medline]
PHST- 2003/11/25 05:00 [entrez]
PHST- 2004/11/01 00:00 [pmc-release]
AID - 1746 [pii]
AID - 10.1046/j.1365-2567.2003.01746.x [doi]
PST - ppublish
SO  - Immunology. 2003 Nov;110(3):322-8. doi: 10.1046/j.1365-2567.2003.01746.x.