Early pregnancy factor suppresses experimental autoimmune encephalomyelitis induced in Lewis rats with myelin basic protein and in SJL/J mice with myelin proteolipid protein peptide 139-151

ZhangB, HarnessJ, Somodevilla-TorresMJ, HillyardNC, MouldAW, AlewoodD, LoveSG, AlewoodPF, GreerJM, CavanaghAC, McCombe, PA, MortonH and RPLisak (2000) Early pregnancy factor suppresses experimental autoimmune encephalomyelitis induced in Lewis rats with myelin basic protein and in SJL/J mice with myelin proteolipid protein peptide 139-151. Journal of the Neurological Sciences, 182 1: 5-15. doi:10.1016/S0022-510X(00)00432-9


Author ZhangB
HarnessJ
Somodevilla-TorresMJ
HillyardNC
MouldAW
AlewoodD
LoveSG
AlewoodPF
GreerJM
CavanaghAC
McCombe, PA
MortonH
RPLisak
Title Early pregnancy factor suppresses experimental autoimmune encephalomyelitis induced in Lewis rats with myelin basic protein and in SJL/J mice with myelin proteolipid protein peptide 139-151
Journal name Journal of the Neurological Sciences   Check publisher's open access policy
ISSN 0022-510X
Publication date 2000-01-01
Year available 2000
Sub-type Article (original research)
DOI 10.1016/S0022-510X(00)00432-9
Open Access Status
Volume 182
Issue 1
Start page 5
End page 15
Total pages 11
Place of publication Shannon, Ireland
Publisher Elsevier Science B.V.
Language eng
Subject C1
320207 Autoimmunity
730102 Immune system and allergy
730104 Nervous system and disorders
Abstract Early pregnancy factor (EPF) is a secreted protein with immunosuppressive and growth factor properties. During pregnancy, it appears in maternal serum within 6-24 h of fertilization, is present for at least the first two-thirds of pregnancy in all species studied and is essential for embryonic survival. It is a homologue of chaperonin 10, a heat shock protein, but, unlike other members of this family, EPF has an extracellular role. As it has the ability to modulate CD4+ T cell-dependent immune responses, its role in treatment of experimental autoimmune encephalomyelitis (EAE) was investigated. EAE is a CD4+ T cell-mediated disease, the best available animal model of multiple sclerosis (MS). Two models of EAE were investigated, acute EAE induced in Lewis rats by inoculation with myelin basic protein (MBP-EAE) and chronic relapsing EAE induced in SJL/J mice by inoculation with myelin proteolipid protein peptide (residues 139-151) (PLP-EAE). EPF, delivered intraperitoneally or orally to rats or intraperitoneally to mice, suppressed clinical signs of disease. Mice with PLP-EAE were also treated with interferon-beta, with and without EPF. Both EPF and IFN-beta suppressed clinical signs of EAE and, when administered together, gave greater suppression than when given separately. These findings suggest that EPF may be a potential candidate for use in treatment of MS and may be of use in combined therapy with IFN-beta. (C) 2000 Elsevier Science B.V. All rights reserved.
Keyword Clinical Neurology
Neurosciences
Chaperonin 10
Experimental Allergic Encephalomyelitis
Heat Shock Protein
Immunoregulation
Multiple Sclerosis
Recombinant Early Pregnancy Factor
Rosette Inhibition Test
Heat-shock Proteins
Multiple-sclerosis
Chaperonin-10 Homolog
Interferon-beta
Identification
Expression
Antibodies
Arthritis
Q-Index Code C1
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Institute for Molecular Bioscience - Publications
 
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Created: Tue, 10 Jun 2008, 20:33:18 EST