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Host-Residual Invariant NK T Cells Attenuate Graft-versus-Host Immunity¹

Kyoko Haraguchi^*,, Tsuyoshi Takahashi^*,2, Akihiko Matsumoto^*,, Takashi Asai^*, Yoshinobu Kanda^*,, Mineo Kurokawa^*, Seishi Ogawa^*,, Hideaki Oda, Masaru Taniguchi^¶, Hisamaru Hirai^3,*, and Shigeru Chiba^4,*,

Departments of^* Hematology/Oncology, Cell Therapy/Transplantation Medicine, and Regeneration Medicine for Hematopoiesis, University of Tokyo Graduate School of Medicine and Hospital, Tokyo, Japan; Department of Pathology, Tokyo Women’s Medical University, Tokyo, Japan; and ^¶ RIKEN Research Center for Allergy and Immunology, Yokohama, Japan

Invariant NK T (iNKT) cells have an invariant TCR- chain and are activated in a CD1d-restricted manner. They are thought to regulate immune responses and play important roles in autoimmunity, allergy, infection, and tumor immunity. They also appear to influence immunity after hemopoietic stem cell transplantation. In this study, we examined the role of iNKT cells in graft-vs-host disease (GVHD) and graft rejection in a mouse model of MHC-mismatched bone marrow transplantation, using materials including -galactosylceramide, NKT cells expanded in vitro, and J18 knockout mice that lack iNKT cells. We found that host-residual iNKT cells constitute effector cells which play a crucial role in reducing the severity of GVHD, and that this reduction is associated with a delayed increase in serum Th2 cytokine levels. Interestingly, we also found that host-residual iNKT cause a delay in engraftment and, under certain conditions, graft rejection. These results indicate that host-residual iNKT cells attenuate graft-vs-host immunity rather than host-vs-graft immunity.

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