Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation.

Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation. Abstract Text:

Lori McCoy,Ikuo Tsunoda,Robert S Fujinami,Lori McCoy,Ikuo Tsunoda,Robert S Fujinami,

Polymicrobial infections have been associated with plausible immune mediated diseases, including multiple sclerosis (MS). Virus infection can prime autoimmune T cells specific for central nervous system (CNS) antigens, if virus has molecular mimicry with CNS proteins. On the other hand, infection of irrelevant viruses will induce two types of cytokine responses. Infection with a virus such as lymphocytic choriomeningitis virus (LCMV), can induce interferon (IFN)-alpha/beta production and suppress autoimmunity, while infection with a virus, such as murine cytomegalovirus (MCMV), can activate natural killer (NK), NKT and dendritic cells, resulting in interleukin (IL)-12 and IFN-gamma production. These cytokines can cause bystander activation of autoreactive T cells. We established an animal model, where mice infected with vaccinia virus encoding myelin protein can mount autoimmune responses. However, the mice develop clinical disease only after irrelevant immune activation either with complete Freund's adjuvant or MCMV infection. In this review, we propose that a combination of two mechanisms, molecular mimicry and bystander activation, induced by virus infection, can lead to CNS demyelinating diseases, including MS. Viral proteins having molecular mimicry with self-proteins in the CNS can prime genetically susceptible individuals. Once this priming has occurred, an immunologic challenge could result in disease through bystander activation by cytokines.

Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation. Publishing Authors By Initials

L McCoy,I Tsunoda,RS Fujinami,L McCoy,I Tsunoda,RS Fujinami,

For similar virus diseases research abstracts see: virus diseases research

PUBMED ID PMID:

MEDLINE DATE:

Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation. Journal Published:

PUBLICATION TYPE: Review

Journal: Autoimmunity

VOLUME: 39

Page Numbers: 9-19

Journal Abbreviation: Autoimmunity

ISSN: 0891-6934

DAY: 1

MONTH: Feb

YEAR: 2006

Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation. Information

Number of References: 119

LANGUAGE: eng

NlmUniqueID: 8900070

Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation. Keywords Mesh Terms:

KEYWORDS: Virus Diseases

MESH TERMS: immunology

Chemical & Substance for Abstract: Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation.

AFFILIATION: University of Utah School of Medicine, Department of Neurology, 30 North 1900 East, Room 3R330, Salt Lake City, UT 84132-2305, USA.

Country: England

AGENCY: United States NIAID

GRANT: AI581501

ACRONYM: AI

MEDLINETA: Autoimmunity

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation Related Publications

• Are There Enhanced MBP Autoantibodies in Autism?
• Are there altered antibody responses to measles, mumps, or rubella viruses in autism?
• Contrasting roles for axonal degeneration in an autoimmune versus viral model of multiple sclerosis: When can axonal injury be beneficial?
• Cross-reactive myelin antibody induces renal pathology.
• How Relevant are GFAP Autoantibodies in Autism and Tourette Syndrome?
• Infectious RNA isolated from the spinal cords of mice chronically infected with Theiler's murine encephalomyelitis virus.
• Inflammation, demyelination, neurodegeneration and neuroprotection in the pathogenesis of multiple sclerosis.
• Modulation of experimental autoimmune encephalomyelitis by VLA-2 blockade.
• Molecular mimicry in multiple sclerosis.
• Multiple sclerosis and virus induced immune responses: autoimmunity can be primed by molecular mimicry and augmented by bystander activation.
• Pathogenic epitopes, heterologous immunity and vaccine design.
• Polyreactive myelin oligodendrocyte glycoprotein antibodies: Implications for systemic autoimmunity in progressive experimental autoimmune encephalomyelitis.
• Regulatory role of CD1d in neurotropic virus infection.
• Role of B:T cell ratio in suppression of clinical signs: A model for silent MS.
• Role of CD5+ B-1 cells in EAE pathogenesis.
• Seizures following picornavirus infection.
• Sequential polymicrobial infections lead to CNS inflammatory disease: possible involvement of bystander activation in heterologous immunity.
• TGF-beta1 suppresses T cell infiltration and VP2 puff B mutation enhances apoptosis in acute polioencephalitis induced by Theiler's virus.
• Targeting inflammatory demyelinating lesions to sites of wallerian degeneration.