Sackler Institute of Graduate Biomedical Sciences, New York University Grossman School of Medicine, New York, NY 10016.
Department of Microbiology, New York University Grossman School of Medicine, New York, NY 10016.
J Immunol. 2020 Jun 15;204(12):3389-3399. doi: 10.4049/jimmunol.1901133. Epub 2020 Apr 29.
Myeloid cells are a vital component of innate immunity and comprise monocytes, macrophages, dendritic cells, and granulocytes. How myeloid cell lineage affects activation states in response to cytokines remains poorly understood. The cytokine environment and cellular infiltrate during an inflammatory response may contain prognostic features that predict disease outcome. In this study, we analyzed the transcriptional responses of human monocytes, macrophages, dendritic cells, and neutrophils in response to stimulation by IFN-γ, IFN-β, IFN-λ, IL-4, IL-13, and IL-10 cytokines to better understand the heterogeneity of activation states in inflammatory conditions. This generated a myeloid cell-cytokine-specific response matrix that can infer representation of myeloid cells and the cytokine environment they encounter during infection, in tumors and in whole blood. Neutrophils were highly responsive to type 1 and type 2 cytokine stimulation but did not respond to IL-10. We identified transcripts specific to IFN-β stimulation, whereas other IFN signature genes were upregulated by both IFN-γ and IFN-β. When we used our matrix to deconvolute blood profiles from tuberculosis patients, the IFN-β-specific neutrophil signature was reduced in tuberculosis patients with active disease, whereas the shared response to IFN-γ and IFN-β in neutrophils was increased. When applied to glioma patients, transcripts of neutrophils exposed to IL-4/IL-13 and monocyte responses to IFN-γ or IFN-β emerged as opposing predictors of patient survival. Hence, by dissecting how different myeloid cells respond to cytokine activation, we can delineate biological roles for myeloid cells in different cytokine environments during disease processes, especially during infection and tumor progression.
髓样细胞是先天免疫的重要组成部分,包括单核细胞、巨噬细胞、树突状细胞和粒细胞。髓样细胞谱系如何影响细胞因子激活状态仍知之甚少。炎症反应期间的细胞因子环境和细胞浸润可能包含预测疾病结局的预后特征。在这项研究中,我们分析了人单核细胞、巨噬细胞、树突状细胞和中性粒细胞对 IFN-γ、IFN-β、IFN-λ、IL-4、IL-13 和 IL-10 细胞因子刺激的转录反应,以更好地了解炎症条件下激活状态的异质性。这产生了一个髓样细胞-细胞因子特异性反应矩阵,可以推断感染、肿瘤和全血中髓样细胞及其遇到的细胞因子环境的代表性。中性粒细胞对 1 型和 2 型细胞因子刺激高度敏感,但对 IL-10 无反应。我们鉴定了对 IFN-β 刺激特异的转录本,而其他 IFN 特征基因则被 IFN-γ 和 IFN-β 上调。当我们使用我们的矩阵来推断结核病患者的血液特征时,在患有活动性疾病的结核病患者中,IFN-β 特异性中性粒细胞特征减少,而中性粒细胞对 IFN-γ 和 IFN-β 的共同反应增加。当应用于神经胶质瘤患者时,暴露于 IL-4/IL-13 的中性粒细胞和单核细胞对 IFN-γ 或 IFN-β 的反应的转录本成为患者生存的相反预测因子。因此,通过剖析不同髓样细胞对细胞因子激活的反应,我们可以描绘出不同细胞因子环境中髓样细胞在疾病过程中的生物学作用,特别是在感染和肿瘤进展期间。