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Blood, 15 November 2007, Vol. 110, No. 10, pp. 3793-3803.
Prepublished online as a Blood First Edition Paper on August 8, 2007; DOI 10.1182/blood-2007-04-086470.
 Previous Article | Next Article 
Submitted April 19, 2007
Accepted July 30, 2007
Regulatory dendritic cells protect against cutaneous chronic graft-versus-
host disease mediated through CD4+CD25+Foxp3+regulatory T cells
Shigeharu Fujita, Yumiko Sato, Kaori Sato, Kawori Eizumi, Tomohiro Fukaya, Masato Kubo, Naohide Yamashita, and Katsuaki Sato*
Laboratory for Dendritic Cell Immunobiology, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan
Laboratory for Signal Network, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan
Department of Advanced Medical Science, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
* Corresponding author; email: katsuaki{at}rcai.riken.jp.
Chronic graft-versus-host disease (cGVHD) is a common cause of morbidity and mortality in allogeneic bone marrow transplantation (alloBMT). However, effective strategies for the treatment of cGVHD have not been established. In this study, we examined the therapeutic utility of modified dendritic cells (DCs) with a greater capacity to regulate immune responses than previously known tolerogenic DCs, regulatory DCs (DCreg), in the major histocompatibility complex (MHC)-compatible and multiple minor histocompatibility antigen (miHAg)-incompatible model of cGVHD in alloBMT. Treatment of the recipient mice following alloBMT with the recipient-type DCreg lead to greater suppression of the incidence and severity of cutaneous cGVHD than rapamycin (RAPA), whereas treatment with the recipient-type mature DCs (mDCs) promoted the pathogenesis. Analysis of the recipient mice suggested that the protective effect of the recipient-type DCreg involved the peripheral generation of alloreactive CD4+CD25+Foxp3+regulatory T (TR) cells from donor-derived CD4+CD25-Foxp3-T cells. Thus, immunotherapy with DCreg is a promising strategy for the treatment of cGVHD in alloBMT mediated through the induction of a dominant tolerance involving CD4+CD25+Foxp3+TR cells.
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