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首页> 外文期刊>Nature immunology >Exacerbated graft-versus-host disease in Pirb~(-/-) mice
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Exacerbated graft-versus-host disease in Pirb~(-/-) mice

机译：Pirb〜（-/-）小鼠加剧了移植物抗宿主病

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摘要

Immune responses are often regulated by opposing receptor pairs that recognize the same ligand but deliver either activating or inhibitory signals. Paired immunoglobulin-like receptors (PIRs) expressed on B cells and myeloid cells comprise a major histocompatibility complex class I recognition system that regulates the responsiveness of these cells. Here, activating PIR-A and inhibitory PIR-B bound various mouse major histocompatibility complex class I (H-2) molecules, and in vitro H-2 tetramer stimulation of PIR-B on B cells or PIR-A on macrophages induced intracellular phosphotyrosine signaling. After transfer of allogeneic splenocytes into PIR-B-deficient mice, the mice showed exacerbated graft-versus-host disease, which was due to augmented activation of recipient dendritic cells with concomitant upregulation of PIR-A and increased interferon-γ production. PIR-A-induced dendritic cell activation also led to increased proliferation of donor cytotoxic T cells. Thus, PIR-A and PIR-B are counteracting receptors that are essential for successful tissue transplantation and may regulate irrelevant reaction to autologous tissues in a constitutive way in physiological conditions.
机译：免疫反应通常由识别相同配体但传递激活或抑制信号的相对受体对调节。在B细胞和髓样细胞上表达的成对的免疫球蛋白样受体（PIR）构成了主要的组织相容性复杂的I类识别系统，该系统调节这些细胞的反应能力。在这里，激活PIR-A和抑制性PIR-B绑定了各种小鼠主要组织相容性复合体I类（H-2）分子，并在体外H-2四聚体刺激了B细胞上的PIR-B或巨噬细胞上的PIR-A诱导了细胞内磷酸酪氨酸信号。将同种异体脾脏细胞转移至PIR-B缺陷型小鼠后，小鼠表现出加剧的移植物抗宿主病，这是由于受体树突状细胞的活化增强，同时伴随PIR-A的上调和干扰素-γ的产生。 PIR-A诱导的树突状细胞活化还导致供体细胞毒性T细胞的增殖增加。因此，PIR-A和PIR-B是抵消受体，它们对于成功的组织移植是必不可少的，并且可以在生理条件下以组成性方式调节与自体组织无关的反应。

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