PMID- 11241588
OWN - NLM
STAT- MEDLINE
DCOM- 20010517
LR  - 20061115
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 63
IP  - 6
DP  - 2001 Mar 15
TI  - Distribution in ocular structures and optic pathways of immunocompetent and glial 
      cells in an experimental allergic encephalomyelitis (EAE) relapsing model.
PG  - 525-35
AB  - Relapsing experimental allergic encephalomyelitis (EAE) was induced in DA rats 
      and the ocular pathologic events were examined at the various phases of the 
      illness. About 80% of EAE rats presented anterior uveitis (AU), even after 
      complete EAE recovery. We studied the phenotype and localization of 
      immunocompetent cells, the major histocompatibility complex (MHC) class I and II 
      antigen expression, as well as the chemokine monocyte chemoattractant protein-1 
      (MCP-1) appearance. In control animals, there were many glial fibrillary acidic 
      protein (GFAP)(+) cells and OX42(+) cells in the ciliary body, retina, optic 
      nerve and chiasma. Except in retina, we observed constitutive MHC class I and II 
      expression. During the EAE acute phase, there was up-regulation of MHC class II 
      and GFAP antigens in iris, ciliary body, limbus, and optic pathways. MHC class I 
      and ED2 antigens were expressed in meninges and in the prechiasmatic cisterna, by 
      cells which could have a role in immune surveillance. MCP-1 mRNA was highly 
      expressed in optic pathways during the acute phase and the protein was expressed 
      by astrocytes, macrophages, and lymphocytes. During the relapsing phase, MCP-1 
      was weakly expressed to disappear almost completely during the final recovery 
      phase. The expression of MHC class II on astrocytes was increased during the 
      relapsing and final recovery phase in which the inflammatory lesions persisted. 
      These findings suggest that ocular areas and optic pathways, mainly optic 
      chiasma, are important targets in the relapsing EAE.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Villarroya, H
AU  - Villarroya H
AD  - Centre Biomedical des Cordeliers, INSERM U 450, Paris, France.
FAU - Klein, C
AU  - Klein C
FAU - Thillaye-Goldenberg, B
AU  - Thillaye-Goldenberg B
FAU - Eclancher, F
AU  - Eclancher F
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Histocompatibility Antigens Class II)
SB  - IM
MH  - Animals
MH  - Antigen Presentation/immunology
MH  - Astrocytes/chemistry/immunology/*pathology
MH  - Blood-Brain Barrier/immunology
MH  - Chemokine CCL2/genetics/immunology
MH  - Disease Models, Animal
MH  - Encephalomyelitis, Autoimmune, Experimental/immunology/*pathology
MH  - Gene Expression/immunology
MH  - Glial Fibrillary Acidic Protein/analysis
MH  - Histocompatibility Antigens Class II/genetics/immunology
MH  - Immunocompetence/physiology
MH  - Male
MH  - Multiple Sclerosis, Relapsing-Remitting/immunology/*pathology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Visual Pathways/immunology/*pathology
EDAT- 2001/03/10 10:00
MHDA- 2001/05/18 10:01
CRDT- 2001/03/10 10:00
PHST- 2001/03/10 10:00 [pubmed]
PHST- 2001/05/18 10:01 [medline]
PHST- 2001/03/10 10:00 [entrez]
AID - 10.1002/jnr.1047 [doi]
PST - ppublish
SO  - J Neurosci Res. 2001 Mar 15;63(6):525-35. doi: 10.1002/jnr.1047.