B cells move to centre stage: novel opportunities for autoimmune disease treatment

被引:222
作者
Browning, Jeffrey L. [1 ]
机构
[1] Biogen Idec Inc, Dept Immunobiol, Cambridge, MA 02445 USA
关键词
D O I
10.1038/nrd2085
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The B-cell arm of the immune system has long been appreciated for its crucial role in pathogen resistance, but in the study of many autoimmune diseases, T cells have dominated the limelight for decades. However, the development of the B-cell-depleting antibody rituximab as a lymphoma therapy has provided a tool to probe the contribution made by B cells in several immune disorders. Recently, the success of B-cell depletion with rituximab in the treatment of rheumatoid arthritis has stimulated investigation of its effects in several other immune disorders, and considerable interest in the potential of drugs that can modulate B-cell function for the treatment of such diseases in general. This article discusses the role of B cells in a range of autoimmune disorders, including rheumatoid arthritis and systemic lupus erythematosus, and analyses approaches to therapeutic B-cell manipulation.
引用
收藏
页码:564 / 576
页数:13
相关论文
共 174 条
[1]   Lymphoid neogenesis in chronic inflammatory diseases [J].
Aloisi, F ;
Pujol-Borrell, R .
NATURE REVIEWS IMMUNOLOGY, 2006, 6 (03) :205-217
[2]   Rituximab improves peripheral B cell abnormalities in human systemic lupus erythematosus [J].
Anolik, JH ;
Barnard, J ;
Cappione, A ;
Pugh-Bernard, AE ;
Felgar, RE ;
Looney, RJ ;
Sanz, I .
ARTHRITIS AND RHEUMATISM, 2004, 50 (11) :3580-3590
[3]   The relationship of FcγRIIIa genotype to degree of B cell depletion by rituximab in the treatment of systemic lupus erythematosus [J].
Anolik, JH ;
Campbell, D ;
Felgar, RE ;
Young, F ;
Sanz, I ;
Rosenblatt, J ;
Looney, RJ .
ARTHRITIS AND RHEUMATISM, 2003, 48 (02) :455-459
[4]   Development of autoantibodies before the clinical onset of systemic lupus erythematosus [J].
Arbuckle, MR ;
McClain, MT ;
Rubertone, MV ;
Scofield, RH ;
Dennis, GJ ;
James, JA ;
Harley, JB .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (16) :1526-1533
[5]   Gene expression profiling in human autoimmunity [J].
Baechler, EC ;
Batliwalla, FM ;
Reed, AM ;
Peterson, EJ ;
Gaffney, PM ;
Moser, KL ;
Gregersen, PK ;
Behrens, TW .
IMMUNOLOGICAL REVIEWS, 2006, 210 :120-137
[6]   Autoimmunity through cytokine-induced dendritic cell activation [J].
Banchereau, J ;
Pascual, V ;
Palucka, AK .
IMMUNITY, 2004, 20 (05) :539-550
[7]   Association of CXCL13 and CCL21 expression with the progressive organization of lymphoid-like structures in Sjogren's syndrome [J].
Barone, F ;
Bombardieri, M ;
Manzo, A ;
Blades, MC ;
Morgan, PR ;
Challacombe, SJ ;
Valesini, G ;
Pitzalis, C .
ARTHRITIS AND RHEUMATISM, 2005, 52 (06) :1773-1784
[8]   Nucleic acids of mammalian origin can act as endogenous ligands for toll-like receptors and may promote systemic lupus erythematosus [J].
Barrat, FJ ;
Meeker, T ;
Gregorio, J ;
Chan, JH ;
Uematsu, S ;
Akira, S ;
Chang, B ;
Duramad, O ;
Coffman, RL .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 202 (08) :1131-1139
[9]   Inherent specificities in natural antibodies: a key to immune defense against pathogen invasion [J].
Baumgarth, N ;
Tung, JW ;
Herzenberg, LA .
SPRINGER SEMINARS IN IMMUNOPATHOLOGY, 2005, 26 (04) :347-362
[10]   Autoreactivity by design: Innate B and T lymphocytes [J].
Bendelac, A ;
Bonneville, M ;
Kearney, JF .
NATURE REVIEWS IMMUNOLOGY, 2001, 1 (03) :177-186