PMID- 12098510
OWN - NLM
STAT- MEDLINE
DCOM- 20020813
LR  - 20190826
IS  - 0165-5728 (Print)
IS  - 0165-5728 (Linking)
VI  - 128
IP  - 1-2
DP  - 2002 Jul
TI  - Upregulation of monocyte chemotactic protein-1 and CC chemokine receptor 2 in the 
      central nervous system is closely associated with relapse of autoimmune 
      encephalomyelitis in Lewis rats.
PG  - 49-57
AB  - Experimental autoimmune encephalomyelitis (EAE) is a disease model of multiple 
      sclerosis (MS) that is characterized by remittance and relapse of the disease and 
      autoimmune and demyelinating lesions in the central nervous system (CNS). To 
      better understand the mechanism of disease relapse, we induced acute and chronic 
      relapsing (CR)-EAE in Lewis rats and examined the differences between the two 
      groups. An immunohistochemical study revealed that significantly higher numbers 
      of macrophages infiltrated the spinal cord during the first and second attacks of 
      CR-EAE than at the peak of acute EAE, whereas the number of infiltrating T cells 
      was essentially the same in acute and CR-EAE. In accordance with this finding, 
      monocyte chemoattractant protein-1 (MCP-1) mRNA, but not MIP-1alpha and RANTES 
      mRNA, increased significantly in CR-EAE lesions rather than in acute EAE lesions. 
      More importantly, the level of MCP-1 during the remission of CR-EAE was 
      significantly higher than during the recovery phase of acute EAE, suggesting that 
      this high level of MCP-1 in CR-EAE is associated with relapse of the disease. CC 
      chemokine receptor 2 (CCR2), the main receptor for MCP-1, was expressed on 
      astrocytes, macrophages and T cells and the number of positive cells was higher 
      in CR-EAE than in acute EAE. Collectively, these findings suggest that high 
      expression of MCP-1 and its receptor, CCR2, in the CNS play important roles in 
      relapse of EAE.
FAU - Jee, Youngheun
AU  - Jee Y
AD  - Department of Molecular Neuropathology, Tokyo Metropolitan Institute for 
      Neuroscience, Musashidai 2-6 Fuchu, Tokyo 183-8526, Japan.
FAU - Yoon, Won Kee
AU  - Yoon WK
FAU - Okura, Yoshio
AU  - Okura Y
FAU - Tanuma, Naoyuki
AU  - Tanuma N
FAU - Matsumoto, Yoh
AU  - Matsumoto Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
RN  - 0 (Ccr2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Ectodysplasins)
RN  - 0 (Membrane Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Antigen, T-Cell, alpha-beta)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Astrocytes/immunology/metabolism
MH  - Central Nervous System/cytology/*immunology/metabolism
MH  - Chemokine CCL2/*genetics
MH  - Chemokines/immunology/metabolism
MH  - Chemotaxis, Leukocyte/*immunology
MH  - Chronic Disease
MH  - Cytokines/immunology/metabolism
MH  - Ectodysplasins
MH  - Encephalomyelitis, Autoimmune, 
      Experimental/*immunology/metabolism/physiopathology
MH  - Endothelium/immunology/metabolism
MH  - Macrophages/immunology/metabolism
MH  - Membrane Proteins/immunology/metabolism
MH  - Multiple Sclerosis/*immunology/metabolism/physiopathology
MH  - RNA, Messenger/immunology/metabolism
MH  - Rats
MH  - Rats, Inbred Lew
MH  - Receptors, Antigen, T-Cell, alpha-beta/immunology/metabolism
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/*genetics
MH  - T-Lymphocytes/immunology/metabolism
MH  - Up-Regulation/*immunology
EDAT- 2002/07/06 10:00
MHDA- 2002/08/14 10:01
CRDT- 2002/07/06 10:00
PHST- 2002/07/06 10:00 [pubmed]
PHST- 2002/08/14 10:01 [medline]
PHST- 2002/07/06 10:00 [entrez]
AID - S0165572802001479 [pii]
AID - 10.1016/s0165-5728(02)00147-9 [doi]
PST - ppublish
SO  - J Neuroimmunol. 2002 Jul;128(1-2):49-57. doi: 10.1016/s0165-5728(02)00147-9.