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The major histocompatibility complex influences the ethiopathogenesis of MS-like disease in primates at multiple levels

Identifieur interne : 001896 ( Main/Exploration ); précédent : 001895; suivant : 001897

The major histocompatibility complex influences the ethiopathogenesis of MS-like disease in primates at multiple levels

Auteurs : Bert A. Hart [Pays-Bas] ; Herbert P. M Brok [Pays-Bas] ; Sandra Amor [Pays-Bas] ; Ronald E. Bontrop [Pays-Bas]

Source :

Human Immunology [ 0198-8859 ] ; 2001.

RBID : ISTEX:6809C60646F6B1EE6E5D50BC6D4CF09BC3D0928B

English descriptors

Abstract

Abstract: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease primarily affecting the central nervous system. Of the many candidate polymorphic major histocompatibility complex (MHC) and non-MHC genes contributing to disease susceptibility, including those encoding effector (cytokines and chemokines) or receptor molecules within the immune system (MHC, TCR, Ig or FcR), human leukocyte antigen (HLA) class II genes have the most significant influence. In this article we put forward the hypothesis that the influence of HLA genes on the risk to develop MS is actually the sum of multiple antigen presenting cell (APC) and T-cell interactions involving HLA class I and class II molecules. This article will also discuss that, because of the genetic and immunologic similarity to humans, autoimmune models of MS in non-human primates are the experimental models “par excellence” to test this hypothesis.

Url:

https://api.istex.fr/ark:/67375/6H6-78BC1HP5-G/fulltext.pdf

DOI: 10.1016/S0198-8859(01)00346-9

Affiliations:

Pays-Bas

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>APC</term>
<term>BBB</term>
<term>CLN</term>
<term>CNS</term>
<term>EAE</term>
<term>HLA</term>
<term>Ig</term>
<term>MBP</term>
<term>MHC</term>
<term>MOG</term>
<term>MS</term>
<term>PLP</term>
<term>SFV</term>
<term>TCR</term>
<term>TMEV</term>
<term>experimental autoimmune encephalomyelitis</term>
<term>immunology</term>
<term>multiple sclerosis</term>
<term>primates</term>
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<keywords scheme="Teeft" xml:lang="en"><term>Adoptive transfer</term>
<term>Allelic lineages</term>
<term>American society</term>
<term>Animal species</term>
<term>Antibodies binding</term>
<term>Antimyelin reactivity</term>
<term>Autoimmune</term>
<term>Autoimmune demyelinating disease</term>
<term>Autoimmune disease</term>
<term>Autoimmune diseases</term>
<term>Autoimmune encephalomyelitis</term>
<term>Autoimmune models</term>
<term>Autoimmune reactions</term>
<term>Autoreactive</term>
<term>Blood brain barrier</term>
<term>Bontrop</term>
<term>Brain barrier</term>
<term>Callithrix jacchus</term>
<term>Cervical lymph nodes</term>
<term>Chronic course</term>
<term>Clin</term>
<term>Clinical heterogeneity</term>
<term>Clinical signs</term>
<term>Common marmoset</term>
<term>Common marmosets</term>
<term>Complement factors</term>
<term>Complete adjuvant</term>
<term>Costimulatory molecules</term>
<term>Cytokine</term>
<term>Cytokine receptors</term>
<term>Demyelination</term>
<term>Disease susceptibility</term>
<term>Elsevier science</term>
<term>Encephalomyelitis</term>
<term>Endothelial cells</term>
<term>Epitope</term>
<term>Etiologic agent</term>
<term>Glycoprotein</term>
<term>Herpes simplex virus</term>
<term>High responsiveness</term>
<term>Histocompatibility</term>
<term>Human immunology</term>
<term>Human leukocyte antigen</term>
<term>Immune</term>
<term>Immune system</term>
<term>Immunol</term>
<term>Immunol today</term>
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<term>Individual animals</term>
<term>Inflammatory demyelination</term>
<term>Influences disease</term>
<term>Interstitial fluids</term>
<term>Laman</term>
<term>Lassmann</term>
<term>Latent infection</term>
<term>Lesion</term>
<term>Lesion formation</term>
<term>Lymphocyte</term>
<term>Macaca mulatta</term>
<term>Major histocompatibility</term>
<term>Marmoset</term>
<term>Marmoset monkeys</term>
<term>Microglia cells</term>
<term>Mimicry</term>
<term>Mimicry epitope</term>
<term>Mimicry motif</term>
<term>Mimicry motifs</term>
<term>Molecular mimicry</term>
<term>Monoclonal antibodies</term>
<term>Multiple sclerosis</term>
<term>Multiple sclerosis patients</term>
<term>Myelin</term>
<term>Myelin antigens</term>
<term>Myelin damage</term>
<term>Myelin epitopes</term>
<term>Myelin formation</term>
<term>Myelin sheaths</term>
<term>Neurol</term>
<term>Neurologic</term>
<term>Neurologic deficit</term>
<term>Node</term>
<term>Nonhuman primates</term>
<term>Nonmyelin antigens</term>
<term>Oligodendrocyte</term>
<term>Pathogenesis</term>
<term>Pathogenic role</term>
<term>Peptide</term>
<term>Peripheral lymph nodes</term>
<term>Persistent infection</term>
<term>Polymorphism</term>
<term>Primary cause</term>
<term>Primary lesion</term>
<term>Primate</term>
<term>Primate model</term>
<term>Primate models</term>
<term>Primates</term>
<term>Proc natl acad</term>
<term>Receptor</term>
<term>Rhesus</term>
<term>Rhesus macaques</term>
<term>Rhesus monkeys</term>
<term>Sclerosis</term>
<term>Semliki forest virus</term>
<term>Spinal cord</term>
<term>Susceptibility</term>
<term>Target organ</term>
<term>Tmev model</term>
<term>Variable disease pattern</term>
<term>Viral</term>
<term>Viral antigens</term>
<term>Viral infection</term>
<term>Waal malefyt</term>
<term>Wekerle</term>
<term>White matter</term>
<term>White matter lesions</term>
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<front><div type="abstract" xml:lang="en">Abstract: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease primarily affecting the central nervous system. Of the many candidate polymorphic major histocompatibility complex (MHC) and non-MHC genes contributing to disease susceptibility, including those encoding effector (cytokines and chemokines) or receptor molecules within the immune system (MHC, TCR, Ig or FcR), human leukocyte antigen (HLA) class II genes have the most significant influence. In this article we put forward the hypothesis that the influence of HLA genes on the risk to develop MS is actually the sum of multiple antigen presenting cell (APC) and T-cell interactions involving HLA class I and class II molecules. This article will also discuss that, because of the genetic and immunologic similarity to humans, autoimmune models of MS in non-human primates are the experimental models “par excellence” to test this hypothesis.</div>
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The major histocompatibility complex influences the ethiopathogenesis of MS-like disease in primates at multiple levels

The major histocompatibility complex influences the ethiopathogenesis of MS-like disease in primates at multiple levels

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri