Mannose-binding lectin pathway is not involved in myasthenia gravis pathogenesis

Jing Li; Huibin Qi; Erdem Tüzün; Windy Allman; Vuslat Yilmaz; Shamsher S. Saini; Feza Deymeer; Güher Saruhan-Direskeneli; Premkumar Christadoss

doi:10.1016/j.jneuroim.2008.12.013

Mannose-binding lectin pathway is not involved in myasthenia gravis pathogenesis

Jing Li, Huibin Qi, Erdem Tüzün, Windy Allman, Vuslat Yilmaz, Shamsher S. Saini, Feza Deymeer, Güher Saruhan-Direskeneli, Premkumar Christadoss

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

9 Scopus citations

Abstract

Classical complement pathway factor, C4 is required for experimental autoimmune myasthenia gravis (EAMG) pathogenesis. C4 is also a central component of the mannose binding lectin (MBL) pathway suggesting that this pathway might also be involved in MG pathogenesis. However, MBL gene deficient mice displayed intact anti-acetylcholine receptor (AChR)-immune response and neuromuscular junction (NMJ) IgG and complement accumulation following AChR-immunization. Moreover, no significant difference was observed between the serum MBL levels of 77 anti-AChR antibody positive generalized MG patients and 105 healthy controls. Therefore, MBL pathway does not play a role in EAMG/MG pathogenesis.

Original language	English (US)
Pages (from-to)	40-45
Number of pages	6
Journal	Journal of Neuroimmunology
Volume	208
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2008.12.013
State	Published - Mar 31 2009
Externally published	Yes

Keywords

Autoimmunity
Complement
Lectin pathway
Mannose binding lectin
Myasthenia gravis

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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10.1016/j.jneuroim.2008.12.013

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@article{469a7e7dd0c945c48ecd0035fc498117,

title = "Mannose-binding lectin pathway is not involved in myasthenia gravis pathogenesis",

abstract = "Classical complement pathway factor, C4 is required for experimental autoimmune myasthenia gravis (EAMG) pathogenesis. C4 is also a central component of the mannose binding lectin (MBL) pathway suggesting that this pathway might also be involved in MG pathogenesis. However, MBL gene deficient mice displayed intact anti-acetylcholine receptor (AChR)-immune response and neuromuscular junction (NMJ) IgG and complement accumulation following AChR-immunization. Moreover, no significant difference was observed between the serum MBL levels of 77 anti-AChR antibody positive generalized MG patients and 105 healthy controls. Therefore, MBL pathway does not play a role in EAMG/MG pathogenesis.",

keywords = "Autoimmunity, Complement, Lectin pathway, Mannose binding lectin, Myasthenia gravis",

author = "Jing Li and Huibin Qi and Erdem T{\"u}z{\"u}n and Windy Allman and Vuslat Yilmaz and Saini, {Shamsher S.} and Feza Deymeer and G{\"u}her Saruhan-Direskeneli and Premkumar Christadoss",

note = "Funding Information: This study is supported by Muscular Dystrophy Association and AFM. Funding Information: Erdem T{\"u}z{\"u}n was a recipient of Myasthenia Gravis foundation Osserman/Sosin/McClure Postdoctoral Fellowship and MDA Neuromuscular Disease Research Career Award. ",

year = "2009",

month = mar,

day = "31",

doi = "10.1016/j.jneuroim.2008.12.013",

language = "English (US)",

volume = "208",

pages = "40--45",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

publisher = "Elsevier B.V.",

number = "1-2",

}

TY - JOUR

T1 - Mannose-binding lectin pathway is not involved in myasthenia gravis pathogenesis

AU - Li, Jing

AU - Qi, Huibin

AU - Tüzün, Erdem

AU - Allman, Windy

AU - Yilmaz, Vuslat

AU - Saini, Shamsher S.

AU - Deymeer, Feza

AU - Saruhan-Direskeneli, Güher

AU - Christadoss, Premkumar

N1 - Funding Information: This study is supported by Muscular Dystrophy Association and AFM. Funding Information: Erdem Tüzün was a recipient of Myasthenia Gravis foundation Osserman/Sosin/McClure Postdoctoral Fellowship and MDA Neuromuscular Disease Research Career Award.

PY - 2009/3/31

Y1 - 2009/3/31

N2 - Classical complement pathway factor, C4 is required for experimental autoimmune myasthenia gravis (EAMG) pathogenesis. C4 is also a central component of the mannose binding lectin (MBL) pathway suggesting that this pathway might also be involved in MG pathogenesis. However, MBL gene deficient mice displayed intact anti-acetylcholine receptor (AChR)-immune response and neuromuscular junction (NMJ) IgG and complement accumulation following AChR-immunization. Moreover, no significant difference was observed between the serum MBL levels of 77 anti-AChR antibody positive generalized MG patients and 105 healthy controls. Therefore, MBL pathway does not play a role in EAMG/MG pathogenesis.

AB - Classical complement pathway factor, C4 is required for experimental autoimmune myasthenia gravis (EAMG) pathogenesis. C4 is also a central component of the mannose binding lectin (MBL) pathway suggesting that this pathway might also be involved in MG pathogenesis. However, MBL gene deficient mice displayed intact anti-acetylcholine receptor (AChR)-immune response and neuromuscular junction (NMJ) IgG and complement accumulation following AChR-immunization. Moreover, no significant difference was observed between the serum MBL levels of 77 anti-AChR antibody positive generalized MG patients and 105 healthy controls. Therefore, MBL pathway does not play a role in EAMG/MG pathogenesis.

KW - Autoimmunity

KW - Complement

KW - Lectin pathway

KW - Mannose binding lectin

KW - Myasthenia gravis

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U2 - 10.1016/j.jneuroim.2008.12.013

DO - 10.1016/j.jneuroim.2008.12.013

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AN - SCOPUS:62549135632

SN - 0165-5728

VL - 208

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EP - 45

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

Mannose-binding lectin pathway is not involved in myasthenia gravis pathogenesis

Abstract

Keywords

ASJC Scopus subject areas

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