Induction of myasthenia gravis in HLA transgenic mice by immunization with human acetylcholine receptors

Huan Yang; Elzbieta Goluszko; Chella David; David K. Okita; Bianca Conti-Fine; Teh Sheng Chan; Mathilde A. Poussin; Premkumar Christadoss

doi:10.1196/annals.1254.044

Induction of myasthenia gravis in HLA transgenic mice by immunization with human acetylcholine receptors

Huan Yang
, Elzbieta Goluszko
, Chella David
, David K. Okita
, Bianca Conti-Fine
, Teh Sheng Chan
, Mathilde A. Poussin
, Premkumar Christadoss

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

We utilized HLA transgenic mice to identify the dominant epitopes on the human (H)-AChR α subunit. The cytoplasmic H-AChR peptide α320-337 was the dominant T cell epitope for DQ8, DR3, and DQ8XDQ6 F1 mice. The H-AChR-immunized HLA-DQ8, DR3, DQ8XDR3 F1 and DQ8XDQ6 F1 mice developed clinical EAMG, whereas HLA-DQ6 mice were less susceptible.

Original language	English (US)
Pages (from-to)	375-378
Number of pages	4
Journal	Annals of the New York Academy of Sciences
Volume	998
DOIs	https://doi.org/10.1196/annals.1254.044
State	Published - 2003
Externally published	Yes

Keywords

AChR
Experimental autoimmune myasthenia gravis (EAMG)
HLA transgenic mice
Myasthenia gravis (MG)

ASJC Scopus subject areas

General Neuroscience
General Biochemistry, Genetics and Molecular Biology
History and Philosophy of Science

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10.1196/annals.1254.044

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title = "Induction of myasthenia gravis in HLA transgenic mice by immunization with human acetylcholine receptors",

abstract = "We utilized HLA transgenic mice to identify the dominant epitopes on the human (H)-AChR α subunit. The cytoplasmic H-AChR peptide α320-337 was the dominant T cell epitope for DQ8, DR3, and DQ8XDQ6 F1 mice. The H-AChR-immunized HLA-DQ8, DR3, DQ8XDR3 F1 and DQ8XDQ6 F1 mice developed clinical EAMG, whereas HLA-DQ6 mice were less susceptible.",

keywords = "AChR, Experimental autoimmune myasthenia gravis (EAMG), HLA transgenic mice, Myasthenia gravis (MG)",

author = "Huan Yang and Elzbieta Goluszko and Chella David and Okita, \{David K.\} and Bianca Conti-Fine and Chan, \{Teh Sheng\} and Poussin, \{Mathilde A.\} and Premkumar Christadoss",

year = "2003",

doi = "10.1196/annals.1254.044",

language = "English (US)",

volume = "998",

pages = "375--378",

journal = "Annals of the New York Academy of Sciences",

issn = "0077-8923",

publisher = "John Wiley and Sons Inc.",

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TY - JOUR

T1 - Induction of myasthenia gravis in HLA transgenic mice by immunization with human acetylcholine receptors

AU - Yang, Huan

AU - Goluszko, Elzbieta

AU - David, Chella

AU - Okita, David K.

AU - Conti-Fine, Bianca

AU - Chan, Teh Sheng

AU - Poussin, Mathilde A.

AU - Christadoss, Premkumar

PY - 2003

Y1 - 2003

N2 - We utilized HLA transgenic mice to identify the dominant epitopes on the human (H)-AChR α subunit. The cytoplasmic H-AChR peptide α320-337 was the dominant T cell epitope for DQ8, DR3, and DQ8XDQ6 F1 mice. The H-AChR-immunized HLA-DQ8, DR3, DQ8XDR3 F1 and DQ8XDQ6 F1 mice developed clinical EAMG, whereas HLA-DQ6 mice were less susceptible.

AB - We utilized HLA transgenic mice to identify the dominant epitopes on the human (H)-AChR α subunit. The cytoplasmic H-AChR peptide α320-337 was the dominant T cell epitope for DQ8, DR3, and DQ8XDQ6 F1 mice. The H-AChR-immunized HLA-DQ8, DR3, DQ8XDR3 F1 and DQ8XDQ6 F1 mice developed clinical EAMG, whereas HLA-DQ6 mice were less susceptible.

KW - AChR

KW - Experimental autoimmune myasthenia gravis (EAMG)

KW - HLA transgenic mice

KW - Myasthenia gravis (MG)

UR - https://www.scopus.com/pages/publications/0141504310

UR - https://www.scopus.com/pages/publications/0141504310#tab=citedBy

U2 - 10.1196/annals.1254.044

DO - 10.1196/annals.1254.044

M3 - Article

C2 - 14592899

AN - SCOPUS:0141504310

SN - 0077-8923

VL - 998

SP - 375

EP - 378

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

ER -

Induction of myasthenia gravis in HLA transgenic mice by immunization with human acetylcholine receptors

Abstract

Keywords

ASJC Scopus subject areas

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