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

UR - https://www.scopus.com/pages/publications/39849108917

UR - https://www.scopus.com/pages/publications/39849108917#tab=citedBy

U2 - 10.1016/j.jneuroim.2007.11.005

DO - 10.1016/j.jneuroim.2007.11.005

M3 - Article

C2 - 18207575

AN - SCOPUS:39849108917

SN - 0165-5728

VL - 194

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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