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Multiple sclerosis: MHC associations and therapeutic implications.

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Multiple sclerosis: MHC associations and therapeutic implications. / Holmes, Samantha; Friese, Manuel A.; Siebold, Christian; Jones, E Yvonne; Bell, John; Fugger, Lars.

in: EXPERT REV MOL MED, Jahrgang 7, Nr. 3, 3, 2005, S. 1-17.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Holmes, S, Friese, MA, Siebold, C, Jones, EY, Bell, J & Fugger, L 2005, 'Multiple sclerosis: MHC associations and therapeutic implications.', EXPERT REV MOL MED, Jg. 7, Nr. 3, 3, S. 1-17. <http://www.ncbi.nlm.nih.gov/pubmed/15710050?dopt=Citation>

APA

Holmes, S., Friese, M. A., Siebold, C., Jones, E. Y., Bell, J., & Fugger, L. (2005). Multiple sclerosis: MHC associations and therapeutic implications. EXPERT REV MOL MED, 7(3), 1-17. [3]. http://www.ncbi.nlm.nih.gov/pubmed/15710050?dopt=Citation

Vancouver

Holmes S, Friese MA, Siebold C, Jones EY, Bell J, Fugger L. Multiple sclerosis: MHC associations and therapeutic implications. EXPERT REV MOL MED. 2005;7(3):1-17. 3.

Bibtex

@article{bf741d96d80644d98d49d7716c4f310c,
title = "Multiple sclerosis: MHC associations and therapeutic implications.",
abstract = "Multiple sclerosis (MS) is an autoimmune disease with an important genetic component. The strongest genetic association is with the major histocompatibility complex (MHC) region. Several MHC alleles predispose to the disease, the most prominent of which are certain alleles in the HLA-DR2 haplotype. Functional and structural studies have helped to explain the molecular basis of these associations. Although there is currently no curative treatment for MS, an increased understanding of the disease has aided the design of immunotherapies that act on the immune system more specifically than the longstanding drugs. Many of these therapies work at the antigen-specific level, disrupting the interaction between T-cell receptors and MHC molecules that leads to disease.",
author = "Samantha Holmes and Friese, {Manuel A.} and Christian Siebold and Jones, {E Yvonne} and John Bell and Lars Fugger",
year = "2005",
language = "Deutsch",
volume = "7",
pages = "1--17",
number = "3",

}

RIS

TY - JOUR

T1 - Multiple sclerosis: MHC associations and therapeutic implications.

AU - Holmes, Samantha

AU - Friese, Manuel A.

AU - Siebold, Christian

AU - Jones, E Yvonne

AU - Bell, John

AU - Fugger, Lars

PY - 2005

Y1 - 2005

N2 - Multiple sclerosis (MS) is an autoimmune disease with an important genetic component. The strongest genetic association is with the major histocompatibility complex (MHC) region. Several MHC alleles predispose to the disease, the most prominent of which are certain alleles in the HLA-DR2 haplotype. Functional and structural studies have helped to explain the molecular basis of these associations. Although there is currently no curative treatment for MS, an increased understanding of the disease has aided the design of immunotherapies that act on the immune system more specifically than the longstanding drugs. Many of these therapies work at the antigen-specific level, disrupting the interaction between T-cell receptors and MHC molecules that leads to disease.

AB - Multiple sclerosis (MS) is an autoimmune disease with an important genetic component. The strongest genetic association is with the major histocompatibility complex (MHC) region. Several MHC alleles predispose to the disease, the most prominent of which are certain alleles in the HLA-DR2 haplotype. Functional and structural studies have helped to explain the molecular basis of these associations. Although there is currently no curative treatment for MS, an increased understanding of the disease has aided the design of immunotherapies that act on the immune system more specifically than the longstanding drugs. Many of these therapies work at the antigen-specific level, disrupting the interaction between T-cell receptors and MHC molecules that leads to disease.

M3 - SCORING: Zeitschriftenaufsatz

VL - 7

SP - 1

EP - 17

IS - 3

M1 - 3

ER -