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Updated: Apr 30, 2026
Functional Characterization of Regulatory Macrophages That Inhibit Graft-reactive Immunity
Published on: June 7, 2017
Dexamethasone palmitate ameliorates macrophages-rich graft-versus-host disease by inhibiting macrophage functions
Satoshi Nishiwaki1, Takayuki Nakayama2, Makoto Murata3
1Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan; Japan Society for the Promotion of Science, Japanese Red Cross Nagoya First Hospital, Nagoya, Aichi, Japan; Department of Hematology, Japanese Red Cross Nagoya First Hospital, Nagoya, Aichi, Japan.
Abstract:
Macrophage infiltration of skin GVHD lesions correlates directly with disease severity, but the mechanisms underlying this relationship remain unclear and GVHD with many macrophages is a therapeutic challenge. Here, we characterize the macrophages involved in GVHD and report that dexamethasone palmitate (DP), a liposteroid, can ameliorate such GVHD by inhibiting macrophage functions. We found that host-derived macrophages could exacerbate GVHD in a mouse model through expression of higher levels of pro-inflammatory TNF-α and IFN-γ, and lower levels of anti-inflammatory IL-10 than resident macrophages in mice without GVHD. DP significantly decreased the viability and migration capacity of primary mouse macrophages compared to conventional dexamethasone in vitro. DP treatment on day 7 and day 14 decreased macrophage number, and attenuated GVHD score and subsequent mortality in a murine model. This is the first study to provide evidence that therapy for GVHD should be changed on the basis of infiltrating cell type.
