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Rheumatology Advance Access originally published online on October 27, 2004
Rheumatology 2005 44(2):151-156; doi:10.1093/rheumatology/keh446
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Rheumatology Vol. 44 No. 2 © British Society for Rheumatology 2004; all rights reserved

REVIEW

Prospects for B-cell-targeted therapy in autoimmune disease

J. C. W. Edwards and G. Cambridge

University College London Centre for Rheumatology, London, UK.

Correspondence to: J. C. W. Edwards, Rheumatology, Arthur Stanley House, 40–50 Tottenham Street, London W1T 4NJ, UK.

KEY WORDS: Rituximab, B-cell depletion, Autoimmunity, Rheumatoid arthritis

The first 150 words of the full text of this article appear below.


   Introduction
 
Reasons for targeting B cells in autoimmune disease date back to the discovery of autoantibodies over 50 yr ago [1]. The idea became of practical interest when anti-B cell monoclonal antibodies were developed in the early 1990s [2, 3]. Fortuitously, at about the same time it became clear that B cells are not simply the subordinate foot soldiers of an immune response but may be as important as T cells in its genesis and regulation. Moreover, it seemed possible that B cells might actually be the driving force behind human autoimmunity. The concept of therapeutic B-lymphocyte depletion (BLyD) emerged subsequently in the pages of this journal [4]. Concept was transformed into reality with the use of the anti-CD20 (i.e. anti-B cell) monoclonal antibody rituximab [5–19].

BLyD has provided clear evidence that B-cell targeting has therapeutic potential [5–19]. The evidence . . . [Full Text of this Article]


   The development of B-lymphocyte depletion
 

   The rationale for B-lymphocyte depletion
 
Clinical pathology is antibody-mediated
Removal of B cells might starve T cells of autoantigen-presenting cells
Removal of self-perpetuating B cells responsible for the vicious cycle of antibody production

   The vicious cycle of antibody production
 

   Aberrant cycle engagement: autoantibodies as immunomodulators
 

   What happens to autoimmune responses after BLyD?
 

   Relationship between antibodies and clinical response
 

   Reasons for relapse
 
Practical problems with BLyD with anti-CD20
Alternative strategies

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