Inhibitory IgG receptor FcγRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis

Jing Li; Erdem Tüzün; Xiong Rong Wu; Hui Bin Qi; Windy Allman; Shamsher S. Saini; Premkumar Christadoss

doi:10.1016/j.jneuroim.2007.11.005

Inhibitory IgG receptor FcγRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis

Jing Li, Erdem Tüzün, Xiong Rong Wu, Hui Bin Qi, Windy Allman, Shamsher S. Saini, Premkumar Christadoss

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

5 Scopus citations

Abstract

Deficiency of the inhibitory FcγRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcγRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcγRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcγRIIB KO mice were mildly resistant to EAMG despite preserved anti-AChR antibody production and neuromuscular junction complement deposition capacity. EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4⁺CD25⁺ cell ratios in lymph nodes. Our data suggest that FcγRIIB promotes antibody-mediated autoimmunity.

Original language	English (US)
Pages (from-to)	44-53
Number of pages	10
Journal	Journal of Neuroimmunology
Volume	194
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2007.11.005
State	Published - Feb 2008
Externally published	Yes

Keywords

Autoimmunity
FcγRIIB
IL-10
IL-6
Myasthenia gravis

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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10.1016/j.jneuroim.2007.11.005

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title = "Inhibitory IgG receptor FcγRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis",

abstract = "Deficiency of the inhibitory FcγRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcγRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcγRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcγRIIB KO mice were mildly resistant to EAMG despite preserved anti-AChR antibody production and neuromuscular junction complement deposition capacity. EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4+CD25+ cell ratios in lymph nodes. Our data suggest that FcγRIIB promotes antibody-mediated autoimmunity.",

keywords = "Autoimmunity, FcγRIIB, IL-10, IL-6, Myasthenia gravis",

author = "Jing Li and Erdem T{\"u}z{\"u}n and Wu, {Xiong Rong} and Qi, {Hui Bin} and Windy Allman and Saini, {Shamsher S.} and Premkumar Christadoss",

note = "Funding Information: This study is supported by NIHR21A1049995, Muscular Dystrophy Association, and Advanced Technology Program of Texas Higher Education Coordinating Board.",

year = "2008",

month = feb,

doi = "10.1016/j.jneuroim.2007.11.005",

language = "English (US)",

volume = "194",

pages = "44--53",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

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TY - JOUR

T1 - Inhibitory IgG receptor FcγRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis

AU - Li, Jing

AU - Tüzün, Erdem

AU - Wu, Xiong Rong

AU - Qi, Hui Bin

AU - Allman, Windy

AU - Saini, Shamsher S.

AU - Christadoss, Premkumar

N1 - Funding Information: This study is supported by NIHR21A1049995, Muscular Dystrophy Association, and Advanced Technology Program of Texas Higher Education Coordinating Board.

PY - 2008/2

Y1 - 2008/2

N2 - Deficiency of the inhibitory FcγRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcγRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcγRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcγRIIB KO mice were mildly resistant to EAMG despite preserved anti-AChR antibody production and neuromuscular junction complement deposition capacity. EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4+CD25+ cell ratios in lymph nodes. Our data suggest that FcγRIIB promotes antibody-mediated autoimmunity.

AB - Deficiency of the inhibitory FcγRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcγRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcγRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcγRIIB KO mice were mildly resistant to EAMG despite preserved anti-AChR antibody production and neuromuscular junction complement deposition capacity. EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4+CD25+ cell ratios in lymph nodes. Our data suggest that FcγRIIB promotes antibody-mediated autoimmunity.

KW - Autoimmunity

KW - FcγRIIB

KW - IL-10

KW - IL-6

KW - Myasthenia gravis

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C2 - 18207575

AN - SCOPUS:39849108917

SN - 0165-5728

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SP - 44

EP - 53

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

Inhibitory IgG receptor FcγRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis

Abstract

Keywords

ASJC Scopus subject areas

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