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Review Article

B cell homeostasis and the development of chronic graft-versus-host disease: implications for B cell-depleting therapy

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Pages 19-25 | Received 20 May 2011, Accepted 04 Jul 2011, Published online: 06 Sep 2011
 

Abstract

Chronic graft-versus-host disease (GVHD) is a serious complication that develops frequently in survivors of allogeneic stem cell transplant. Since elucidation of the role of B cells in the pathogenesis of chronic GVHD, B cell-depleting therapy with rituximab has been associated with beneficial effects in clinical and laboratory studies in patients with chronic GVHD. Although the mechanism underlying the contribution of B cells to the development of chronic GVHD is poorly understood, recent studies have proposed that B cell reconstitution after allogeneic stem cell transplant is involved in the development of chronic GVHD. Inadequate reconstitution of naive B cells and the persistence of high levels of B cell-activating factor have been found in patients with chronic GVHD, and these changes might be associated with the expansion of activated CD27-positive B cells that produce autoantibody in chronic GVHD. In the light of this altered B cell homeostasis in chronic GVHD, the role of rituximab in controlling the clinical manifestations of chronic GVHD has been studied. In this review, we address the role of B cells in the pathogenesis of chronic GVHD and the response to B cell-depleting therapy based on B cell homeostasis.

Acknowledgements

This study was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2009-0075642), and the IN-SUNG Foundation for Medical Research (CA98661).

Potential conflict of interest:

Disclosure forms provided by the authors are available with the full text of this article at www.informahealthcare.com/lal.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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