Heat shock proteins and experimental autoimmune encephalomyelitis (EAE): I. Immunization with a peptide of the myelin protein 2',3' cyclic nucleotide 3' phosphodiesterase that is cross-reactive with a heat shock protein alters the course of EAE

G Birnbaum; L Kotilinek; P Schlievert; H B Clark; J Trotter; E Horvath; E Gao; M Cox; P E Braun

doi:10.1002/(SICI)1097-4547(19960515)44:4<381::AID-JNR10>3.0.CO;2-5

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Heat shock proteins and experimental autoimmune encephalomyelitis (EAE): I. Immunization with a peptide of the myelin protein 2',3' cyclic nucleotide 3' phosphodiesterase that is cross-reactive with a heat shock protein alters the course of EAE

Journal article

Peer reviewed

Heat shock proteins and experimental autoimmune encephalomyelitis (EAE): I. Immunization with a peptide of the myelin protein 2',3' cyclic nucleotide 3' phosphodiesterase that is cross-reactive with a heat shock protein alters the course of EAE

G Birnbaum, L Kotilinek, P Schlievert, H B Clark, J Trotter, E Horvath, E Gao, M Cox and P E Braun

Journal of neuroscience research, Vol.44(4), pp.381-396

05/15/1996

DOI: 10.1002/(SICI)1097-4547(19960515)44:4<381::AID-JNR10>3.0.CO;2-5

PMID: 8739158

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Abstract

We describe sequence similarity and immunologic cross-reactivity between a peptide of the mycobacterial hsp, HSP65, and the myelin protein 2',3' cyclic nucleotide 3' phosphodiesterase (CNP). We demonstrate that immunization with the homologous cross-reactive CNP peptide (hsp-CNP peptide) has significant biological consequences. Rats immunized with hsp-CNP peptide in either complete Freund's adjuvant (CFA) or incomplete Freund's adjuvant (IFA) produce large amounts of peptide-specific antibody. Isotypes of antibodies in animals immunized with peptide in CFA are IgG1 and IgG2a. Isotypes of antibodies in rats immunized with peptide in IFA are predominantly IgG1, with low titers of IgG2a. T cell proliferative responses to HSP65 are present in rats immunized with peptide in CFA. T cell responses to HSP65 initially are absent in rats immunized with peptide in IFA but develop over time. T cell proliferative responses to hsp-CNP peptide were not detected. None of the groups of rats developed clinical or histologic evidence of experimental autoimmune encephalomyelitis (EAE). To induce EAE, rats preimmunized with hsp-CNP peptide were challenged with guinea pig spinal cord (GPSC) emulsified in CFA. Rats preimmunized with peptide in CFA developed severe EAE. Rats preimmunized with hsp-CNP peptide in IFA were protected from EAE, with both a lower incidence and severity of disease. Injecting the murine monoclonal antibody recognizing the shared HSP65 and CNP epitope did not protect against EAE. Our data suggest that a Th2 pattern of immune response to a CNP peptide that itself is non-encephalitogenic protects against EAE. Immune responses to either hsp or myelin proteins cross-reactive with hsp may play an important role in the development of EAE.

Humans

Rats, Inbred Lew

Encephalomyelitis, Autoimmune, Experimental - immunology

Molecular Sequence Data

Recombinant Proteins - biosynthesis

Epitopes - immunology

Chaperonin 60

Immunoglobulin G - biosynthesis

Time Factors

2',3'-Cyclic-Nucleotide Phosphodiesterases - immunology

Female

Amino Acid Sequence

Encephalomyelitis, Autoimmune, Experimental - pathology

Guinea Pigs

Myelin Sheath - immunology

Lymphocyte Activation

Rats

Antibodies, Monoclonal

Chaperonins - immunology

Bacterial Proteins

Freund's Adjuvant

Spinal Cord - immunology

Immunoglobulin Isotypes - biosynthesis

Animals

Antibody Formation

Epitopes - chemistry

Mice

Immunity, Cellular

Details

Title: Subtitle: Heat shock proteins and experimental autoimmune encephalomyelitis (EAE): I. Immunization with a peptide of the myelin protein 2',3' cyclic nucleotide 3' phosphodiesterase that is cross-reactive with a heat shock protein alters the course of EAE
Creators: G Birnbaum - Department of Neurology, University of Minnesota, Minneapolis 55455, USA
L Kotilinek
P Schlievert
H B Clark
J Trotter
E Horvath
E Gao
M Cox
P E Braun
Resource Type: Journal article
Publication Details: Journal of neuroscience research, Vol.44(4), pp.381-396
Publisher: United States
DOI: 10.1002/(SICI)1097-4547(19960515)44:4<381::AID-JNR10>3.0.CO;2-5
PMID: 8739158
ISSN: 0360-4012
eISSN: 1097-4547
Language: English
Date published: 05/15/1996
Academic Unit: Microbiology and Immunology; Pathology; Internal Medicine
Record Identifier: 9984001215902771

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