Ectopic germinal centers, BAFF and anti-B-cell therapy in myasthenia gravis

被引：73

作者：

Berrih-Aknin, Sonia ^{[1
]}

Ragheb, Samia ^{[2
]}

Le Panse, Rozen ^{[1
]}

Lisak, Robert P. ^{[3
,4
]}

机构：

[1] Grp Hosp Pitie Salpetriere, Unite Mixte Rech, CNRS UMR7215 INSERM U974 UPMC UM76 AIM Therapie M, F-75651 Paris, France

[2] OUWB, Sch Med, Dept Biomed Sci, Rochester, MI 48309 USA

[3] Wayne State Univ, Sch Med, Dept Neurol & Immunol, Detroit, MI 48201 USA

[4] Wayne State Univ, Sch Med, Dept Microbiol, Detroit, MI 48201 USA

来源：

AUTOIMMUNITY REVIEWS | 2013年 / 12卷 / 09期

关键词：

Myasthenia gravis; B cells; Anti-acetylcholine receptor antibodies; Germinal centers; BAFF; Anti-B-cell therapies; SYSTEMIC-LUPUS-ERYTHEMATOSUS; ANTIACETYLCHOLINE RECEPTOR ANTIBODIES; PRIMARY SJOGRENS-SYNDROME; NECROSIS-FACTOR FAMILY; RITUXIMAB-TREATED PATIENTS; BARR-VIRUS INFECTION; LIVED PLASMA-CELLS; T-CELL; TNF FAMILY; ACETYLCHOLINE-RECEPTOR;

D O I：

10.1016/j.autrev.2013.03.011

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Myasthenia gravis (MG) is an autoimmune disease mediated by antibodies directed to molecules of the endplate of the neuromuscular junction. B cells play a major role in MG disease since they produce the pathogenic antibodies and therapies targeting B cells are effective. The aim of this article was to review the role of B cells in myasthenia gravis. We will first describe what we know about B cells in this disease and examine the involvement of the B cells in the thymus of MG patients. We will detail the role of factors associated with B-cell function such as BAFF. Finally, we will discuss the effects of therapy targeting B cells. (C) 2013 Elsevier B.V. All rights reserved.

引用

页码：885 / 893

页数：9

共 192 条

[1]

Acsadi A, 2010, CURR TREAT OPTION NE, V12, P221

[2]

Aissaoui A, 1999, ANN NEUROL, V46, P559, DOI 10.1002/1531-8249(199910)46:4<559::AID-ANA3>3.0.CO

[3]

2-S

[4] Lymphoid neogenesis in chronic inflammatory diseases [J].

Aloisi, F ;

Pujol-Borrell, R .

NATURE REVIEWS IMMUNOLOGY, 2006, 6 (03) :205-217

[5] THE CD5(+) B-CELLS AND MYASTHENIA-GRAVIS [J].

ARAGA, S ;

KISHIMOTO, M ;

ADACHI, A ;

NAKAYASU, H ;

TAKENAKA, T ;

TAKAHASHI, K .

AUTOIMMUNITY, 1995, 20 (02) :129-134

[6] The role of long-lived plasma cells in autoimmunity -: Review [J].

Arce, S ;

Cassese, G ;

Hauser, A ;

Dörner, T ;

Odendahl, M ;

Manz, R ;

Radbruch, A ;

Hiepe, F .

IMMUNOBIOLOGY, 2002, 206 (05) :558-562

[7] Blocking of IL-6 suppresses experimental autoimmune myasthenia gravis [J].

Aricha, Revital ;

Mizrachi, Keren ;

Fuchs, Sara ;

Souroujon, Miriam C. .

JOURNAL OF AUTOIMMUNITY, 2011, 36 (02) :135-141

[8] The susceptibility of Aire-/- mice to experimental myasthenia gravis involves alterations in regulatory T cells [J].

Aricha, Revital ;

Feferman, Tali ;

Scott, Hamish S. ;

Souroujon, Miriam C. ;

Berrih-Aknin, Sonia ;

Fuchs, Sara .

JOURNAL OF AUTOIMMUNITY, 2011, 36 (01) :16-24

[9] The life span of short-lived plasma cells is partly determined by a block on activation of apoptotic caspases acting in combination with endoplasmic reticulum stress [J].

Auner, Holger W. ;

Beham-Schmid, Christine ;

Dillon, Niall ;

Sabbattini, Pierangela .

BLOOD, 2010, 116 (18) :3445-3455

[10] BAFF selectively enhances the survival of plasmablasts generated from human memory B cells [J].

Avery, DT ;

Kalled, SL ;

Ellyard, JI ;

Ambrose, C ;

Bixler, SA ;

Thien, M ;

Brink, R ;

Mackay, F ;

Hodgkin, PD ;

Tangye, SG .

JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (02) :286-297

← 1 2 3 4 5 6 7 8 9 10 →