In this issue of Blood, Piper et al find that donor T cells that secrete granulocyte-macrophage colony-stimulating factor (GM-CSF) promote graft-versus-host disease (GVHD) by recruiting donor dendritic cells. This amplifies the activation of alloreactive T cells and increases the severity of GVHD. The authors identified GM-CSF secretion in a rare population of CD11c+ CD4+ T cells that express the transcription factor Bhlhe40. Piper et al showed that Bhlhe40+ CD4+ donor T cells are central to the development of GVHD in the gut in murine models of allogeneic bone marrow transplantation (BMT). Transplantation of either GM-CSF or Bhlhe40 knockout donor T cells resulted in significantly lower incidence of GVHD in allogeneic BMT recipients. This paper is of broad interest to hematologists and immunologists as it illuminates the role of donor T cells in activating dendritic cells and positions GM-CSF–producing T cells as a critical link between innate and adaptive immune responses.

中文翻译：

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旧细胞因子的新作用：GM-CSF 放大 GVHD

在本期 Blood 中，Piper 等人发现，分泌粒细胞-巨噬细胞集落刺激因子 (GM-CSF) 的供体 T 细胞通过招募供体树突状细胞来促进移植物抗宿主病 (GVHD)。这会放大同种异体反应性 T 细胞的激活并增加 GVHD 的严重程度。作者在表达转录因子 Bhlhe40 的罕见 CD11c+ CD4+ T 细胞群中发现了 GM-CSF 分泌。Piper 等人表明，在同种异体骨髓移植 (BMT) 的小鼠模型中，Bhlhe40+ CD4+ 供体 T 细胞是肠道 GVHD 发展的核心。GM-CSF 或 Bhlhe40 敲除供体 T 细胞的移植导致同种异体 BMT 受体中 GVHD 的发生率显着降低。