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M-CSF 指导髓样细胞和自然杀伤细胞分化，以在造血细胞移植后防止 CMV 感染。

M-CSF directs myeloid and NK cell differentiation to protect from CMV after hematopoietic cell transplantation.

机构信息

Center for Regenerative Therapies Dresden (CRTD), Technical University Dresden, Dresden, Germany.

Aix Marseille University, CNRS, INSERM, CIML, Marseille, France.

出版信息

EMBO Mol Med. 2023 Nov 8;15(11):e17694. doi: 10.15252/emmm.202317694. Epub 2023 Aug 28.

DOI:10.15252/emmm.202317694
PMID:37635627
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10630876/
Abstract

Therapies reconstituting autologous antiviral immunocompetence may represent an important prophylaxis and treatment for immunosuppressed individuals. Following hematopoietic cell transplantation (HCT), patients are susceptible to Herpesviridae including cytomegalovirus (CMV). We show in a murine model of HCT that macrophage colony-stimulating factor (M-CSF) promoted rapid antiviral activity and protection from viremia caused by murine CMV. M-CSF given at transplantation stimulated sequential myeloid and natural killer (NK) cell differentiation culminating in increased NK cell numbers, production of granzyme B and interferon-γ. This depended upon M-CSF-induced myelopoiesis leading to IL15Rα-mediated presentation of IL-15 on monocytes, augmented by type I interferons from plasmacytoid dendritic cells. Demonstrating relevance to human HCT, M-CSF induced myelomonocytic IL15Rα expression and numbers of functional NK cells in G-CSF-mobilized hematopoietic stem and progenitor cells. Together, M-CSF-induced myelopoiesis triggered an integrated differentiation of myeloid and NK cells to protect HCT recipients from CMV. Thus, our results identify a rationale for the therapeutic use of M-CSF to rapidly reconstitute antiviral activity in immunocompromised individuals, which may provide a general paradigm to boost innate antiviral immunocompetence using host-directed therapies.

摘要

重建自体抗病毒免疫能力的疗法可能代表了一种针对免疫抑制个体的重要预防和治疗方法。造血细胞移植（HCT）后，患者易感染疱疹病毒科，包括巨细胞病毒（CMV）。我们在 HCT 的小鼠模型中表明，巨噬细胞集落刺激因子（M-CSF）可促进快速抗病毒活性，并防止由鼠 CMV 引起的病毒血症。移植时给予 M-CSF 可刺激髓系和自然杀伤（NK）细胞的连续分化，最终导致 NK 细胞数量增加、颗粒酶 B 和干扰素-γ的产生。这取决于 M-CSF 诱导的髓样细胞生成，导致 IL-15 在单核细胞上由 IL15Rα 呈递，这一过程被浆细胞样树突状细胞产生的 I 型干扰素增强。证明与人类 HCT 相关，M-CSF 在 G-CSF 动员的造血干细胞和祖细胞中诱导髓系和 NK 细胞的 IL15Rα 表达和功能 NK 细胞数量增加。总之，M-CSF 诱导的髓样细胞生成触发了髓样细胞和 NK 细胞的整合分化，从而保护 HCT 受者免受 CMV 感染。因此，我们的研究结果为 M-CSF 的治疗应用提供了依据，可快速重建免疫抑制个体的抗病毒活性，这可能为使用宿主定向疗法增强先天抗病毒免疫能力提供了一个普遍的范例。

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