RGD Reference Report - Distribution in ocular structures and optic pathways of immunocompetent and glial cells in an experimental allergic encephalomyelitis (EAE) relapsing model.

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Distribution in ocular structures and optic pathways of immunocompetent and glial cells in an experimental allergic encephalomyelitis (EAE) relapsing model.
Authors:	Villarroya, H Klein, C Thillaye-Goldenberg, B Eclancher, F
Citation:	Villarroya H, etal., J Neurosci Res. 2001 Mar 15;63(6):525-35.
RGD ID:	8548888
Pubmed:	PMID:11241588 (View Abstract at PubMed)
DOI:	DOI:10.1002/jnr.1047 (Journal Full-text)
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.

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Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
Experimental Autoimmune Encephalomyelitis		ISO	Ccl2 (Rattus norvegicus)	8548888; 8548888	mRNA:increased expression:optic chiasma (rat)	RGD
Experimental Autoimmune Encephalomyelitis		IEP		8548888	mRNA:increased expression:optic chiasma (rat)	RGD

Objects Annotated

Genes (Rattus norvegicus)

Ccl2 (C-C motif chemokine ligand 2)

Genes (Mus musculus)

Ccl2 (C-C motif chemokine ligand 2)

Genes (Homo sapiens)

CCL2 (C-C motif chemokine ligand 2)

Objects referenced in this article

Gene	CCL13	C-C motif chemokine ligand 13	Homo sapiens

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Distribution in ocular structures and optic pathways of immunocompetent and glial cells in an experimental allergic encephalomyelitis (EAE) relapsing model.