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Blood, 26 February 2009, Vol. 113, No. 9, pp. 2088-2095.
Prepublished online as a Blood First Edition Paper on January 14, 2009; DOI 10.1182/blood-2008-07-168609.
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Submitted July 14, 2008
Accepted December 30, 2008
Plasmacytoid dendritic cells prime alloreactive T cells to mediate graft-versus-host disease as antigen-presenting cells
Motoko Koyama, Daigo Hashimoto, Kazutoshi Aoyama, Ken-ichi Matsuoka, Kennosuke Karube, Hiroaki Niiro, Mine Harada, Mitsune Tanimoto, Koichi Akashi, and Takanori Teshima*
Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Science, Fukuoka, Japan
Center for Cellular and Molecular Medicine, Kyushu University Hospital, Fukuoka, Japan
Biopathological Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan
Department of Pathology, School of Medicine, Kurume University, Kurume, Japan
* Corresponding author; email: tteshima{at}cancer.med.kyushu-u.ac.jp.
Dendritic cells (DCs) can be classified into two distinct subsets: conventional DCs (cDCs) and plasmacytoid DCs (pDCs). cDCs can prime antigen-specific T cell immunity, whereas in vivo function of pDCs as antigen-presenting cells remains controversial. We evaluated the contribution of pDCs to allogeneic T cell responses in vivo in mouse models of graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation by an add-back study of MHC-expressing pDCs into major histocompatibility complex deficient mice that were resistant to GVHD. Alloantigen expression on pDCs alone was sufficient to prime alloreactive T cells and cause GVHD. An inflammatory environment created by host irradiation has the decisive role in maturing pDCs for T cell priming but this process does not require Toll-like receptor signaling. Thus functional outcomes of pDC-T cell interactions depend on the immunological context of encounter. To our knowledge, these results are the first to directly demonstrate an in vivo pathogenic role of pDCs as antigen-presenting cells in an antigen-specific T-cell-mediated disease in the absence of other DC subsets, and provide important insight into developing strategies for tolerance induction in transplantation.
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