PMID- 20035831
OWN - NLM
STAT- MEDLINE
DCOM- 20100406
LR  - 20100201
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 470
IP  - 1
DP  - 2010 Feb 5
TI  - TNF-alpha receptor 1 deficiency reduces antigen-presenting capacity of Schwann 
      cells and ameliorates experimental autoimmune neuritis in mice.
PG  - 19-23
LID - 10.1016/j.neulet.2009.12.045 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a pleiotropic pro-inflammatory 
      cytokine with potentially neurodestructive effects and plays a pivotal role in 
      autoimmune demyelinating disease. To address the role of TNF-alpha in the 
      pathogenesis of experimental autoimmune neuritis (EAN), the current study 
      investigated the antigen-presenting capacity of Schwann cells (SCs) in EAN 
      induced by P0 protein peptide 106-125 in TNF-alpha receptor 1 deficient 
      (TNFR1(-/-)) mice. The antigen-presenting capacity of SCs was assessed by the 
      expression of MHC class II (MHCII), CD40, CD80 and CD86 molecules on activated 
      SCs as well as by induction of T cell proliferation in co-cultures of P0 protein 
      peptide 106-125 specific T cells with activated SCs. In addition, the expression 
      of inducible nitric oxide synthase (iNOS) was measured in activated SCs by flow 
      cytometry. TNFR1(-/-) EAN mice developed significantly delayed and reduced 
      clinical signs of EAN compared to wild type EAN mice. In parallel, the expression 
      of MHCII, CD80 and iNOS on SCs were decreased in TNFR1(-/-) mice compared to wild 
      type mice. Likewise, proliferation of P0 protein peptide 106-125 specific T cells 
      simulated by activated SCs of TNFR1(-/-) EAN mice was lower than that of wild 
      type EAN mice. Our data suggest that TNF-alpha may exert pro-inflammatory effects 
      in EAN via TNFR1 by up-regulating the antigen-presenting function and iNOS 
      production of SCs.
CI  - (c) 2009 Elsevier Ireland Ltd. All rights reserved.
FAU - Mao, Xi-Jing
AU  - Mao XJ
AD  - Department of Neurology, First Hospital of Jilin University, Changchun, China.
FAU - Zhang, Xing-Mei
AU  - Zhang XM
FAU - Zhang, Hong-Liang
AU  - Zhang HL
FAU - Quezada, Hernan Concha
AU  - Quezada HC
FAU - Mix, Eilhard
AU  - Mix E
FAU - Yang, Xin
AU  - Yang X
FAU - Winblad, Bengt
AU  - Winblad B
FAU - Adem, Abdu
AU  - Adem A
FAU - Zhu, Jie
AU  - Zhu J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091224
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Antigens)
RN  - 0 (Myelin P0 Protein)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tnfrsf1a protein, mouse)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
SB  - IM
MH  - Animals
MH  - Antigens/*metabolism
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Coculture Techniques
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Myelin P0 Protein/metabolism
MH  - Neuritis, Autoimmune, Experimental/*metabolism
MH  - Nitric Oxide Synthase Type II/metabolism
MH  - Receptors, Tumor Necrosis Factor, Type I/deficiency/genetics/*metabolism
MH  - Schwann Cells/enzymology/*metabolism
MH  - T-Lymphocytes/physiology
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2009/12/29 06:00
MHDA- 2010/04/07 06:00
CRDT- 2009/12/29 06:00
PHST- 2009/10/07 00:00 [received]
PHST- 2009/12/03 00:00 [revised]
PHST- 2009/12/18 00:00 [accepted]
PHST- 2009/12/29 06:00 [entrez]
PHST- 2009/12/29 06:00 [pubmed]
PHST- 2010/04/07 06:00 [medline]
AID - S0304-3940(09)01627-9 [pii]
AID - 10.1016/j.neulet.2009.12.045 [doi]
PST - ppublish
SO  - Neurosci Lett. 2010 Feb 5;470(1):19-23. doi: 10.1016/j.neulet.2009.12.045. Epub 
      2009 Dec 24.