Genetic evidence for the involvement of Fcγ receptor III in experimental autoimmune myasthenia gravis pathogenesis

Erdem Tüzün; Shamsher S. Saini; Huan Yang; Dhivyaa Alagappan; Stephen Higgs; Premkumar Christadoss

doi:10.1016/j.jneuroim.2006.01.015

Genetic evidence for the involvement of Fcγ receptor III in experimental autoimmune myasthenia gravis pathogenesis

Erdem Tüzün, Shamsher S. Saini, Huan Yang, Dhivyaa Alagappan, Stephen Higgs, Premkumar Christadoss

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

18 Scopus citations

Abstract

Immune complexes and classical complement pathway play vital roles in experimental autoimmune myasthenia gravis (EAMG). To analyze the role of immune complex receptors in EAMG, FcγRIII knockout (KO) mice were immunized with AChR and were found out to be resistant to EAMG induction. This was associated with reduced neuromuscular junction deposits, lymph node cell (LNC) IL-6 production and serum complement levels. EAMG resistance of anti-C1q Ab-administered mice was also associated with reduced LNC IL-6 production and neuromuscular junction deposits, indicating C1q involvement in EAMG resistance. The data provide the first direct genetic evidence for Fcγ receptor involvement in EAMG pathogenesis.

Original language	English (US)
Pages (from-to)	157-167
Number of pages	11
Journal	Journal of Neuroimmunology
Volume	174
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2006.01.015
State	Published - May 2006
Externally published	Yes

Keywords

Autoimmunity
C1q
Experimental autoimmune myasthenia gravis
Fc receptors
Myasthenia gravis

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

Access to Document

10.1016/j.jneuroim.2006.01.015

Cite this

@article{81f4fe1c23f6429a9634693f81733341,

title = "Genetic evidence for the involvement of Fcγ receptor III in experimental autoimmune myasthenia gravis pathogenesis",

abstract = "Immune complexes and classical complement pathway play vital roles in experimental autoimmune myasthenia gravis (EAMG). To analyze the role of immune complex receptors in EAMG, FcγRIII knockout (KO) mice were immunized with AChR and were found out to be resistant to EAMG induction. This was associated with reduced neuromuscular junction deposits, lymph node cell (LNC) IL-6 production and serum complement levels. EAMG resistance of anti-C1q Ab-administered mice was also associated with reduced LNC IL-6 production and neuromuscular junction deposits, indicating C1q involvement in EAMG resistance. The data provide the first direct genetic evidence for Fcγ receptor involvement in EAMG pathogenesis.",

keywords = "Autoimmunity, C1q, Experimental autoimmune myasthenia gravis, Fc receptors, Myasthenia gravis",

author = "Erdem T{\"u}z{\"u}n and Saini, {Shamsher S.} and Huan Yang and Dhivyaa Alagappan and Stephen Higgs and Premkumar Christadoss",

note = "Funding Information: This study is supported by Muscular Dystrophy Association and Advanced Technology Program of Texas Higher Education Coordinating Board.",

year = "2006",

month = may,

doi = "10.1016/j.jneuroim.2006.01.015",

language = "English (US)",

volume = "174",

pages = "157--167",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

publisher = "Elsevier",

number = "1-2",

}

TY - JOUR

T1 - Genetic evidence for the involvement of Fcγ receptor III in experimental autoimmune myasthenia gravis pathogenesis

AU - Tüzün, Erdem

AU - Saini, Shamsher S.

AU - Yang, Huan

AU - Alagappan, Dhivyaa

AU - Higgs, Stephen

AU - Christadoss, Premkumar

N1 - Funding Information: This study is supported by Muscular Dystrophy Association and Advanced Technology Program of Texas Higher Education Coordinating Board.

PY - 2006/5

Y1 - 2006/5

N2 - Immune complexes and classical complement pathway play vital roles in experimental autoimmune myasthenia gravis (EAMG). To analyze the role of immune complex receptors in EAMG, FcγRIII knockout (KO) mice were immunized with AChR and were found out to be resistant to EAMG induction. This was associated with reduced neuromuscular junction deposits, lymph node cell (LNC) IL-6 production and serum complement levels. EAMG resistance of anti-C1q Ab-administered mice was also associated with reduced LNC IL-6 production and neuromuscular junction deposits, indicating C1q involvement in EAMG resistance. The data provide the first direct genetic evidence for Fcγ receptor involvement in EAMG pathogenesis.

AB - Immune complexes and classical complement pathway play vital roles in experimental autoimmune myasthenia gravis (EAMG). To analyze the role of immune complex receptors in EAMG, FcγRIII knockout (KO) mice were immunized with AChR and were found out to be resistant to EAMG induction. This was associated with reduced neuromuscular junction deposits, lymph node cell (LNC) IL-6 production and serum complement levels. EAMG resistance of anti-C1q Ab-administered mice was also associated with reduced LNC IL-6 production and neuromuscular junction deposits, indicating C1q involvement in EAMG resistance. The data provide the first direct genetic evidence for Fcγ receptor involvement in EAMG pathogenesis.

KW - Autoimmunity

KW - C1q

KW - Experimental autoimmune myasthenia gravis

KW - Fc receptors

KW - Myasthenia gravis

UR - http://www.scopus.com/inward/record.url?scp=33646102469&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33646102469&partnerID=8YFLogxK

U2 - 10.1016/j.jneuroim.2006.01.015

DO - 10.1016/j.jneuroim.2006.01.015

M3 - Article

C2 - 16527362

AN - SCOPUS:33646102469

SN - 0165-5728

VL - 174

SP - 157

EP - 167

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

Genetic evidence for the involvement of Fcγ receptor III in experimental autoimmune myasthenia gravis pathogenesis

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this