Apoptosis in human monocytes: possible role in chronic inflammatory diseases.
Apoptosis in human monocytes: possible role in chronic inflammatory diseases.
复制标题
DOI：
--
复制
发表时间：
1993-05
影响因子：
4.3
通讯作者：
D. Mangan;S. E. Mergenhagen;S. Wahl
中科院分区：
文献类型：
--
作者：
D. Mangan;S. E. Mergenhagen;S. Wahl
细胞凋亡或程序性细胞死亡是细胞自杀的一种生理形式，它受到细胞外微环境的深刻影响。细胞凋亡的特征是一系列导致细胞萎缩的遗传和生化事件，胞浆和核物质凝聚，染色体DNA裂解成寡核小体大小(约200bp)片段，吞噬细胞增强对濒死细胞的识别。细胞凋亡从根本上不同于细胞死亡的病理形式--细胞肿胀和溶解。选择性诱导白细胞凋亡的能力可能是控制这些细胞在炎性病变中聚集的重要生理机制。在这篇文章中，我们回顾了我们关于人类单核细胞凋亡的数据，单核细胞对慢性炎症的持续和消退都有贡献。当单核细胞在没有适当的外源刺激的情况下培养时，可以启动细胞凋亡。例如，添加趋化因子不足以阻止细胞凋亡。然而，单核细胞在血清存在下的黏附、微生物产物如脂多糖或某些促炎细胞因子，如白介素1和肿瘤坏死因子-α，都可以抑制单核细胞的凋亡。来源于1型辅助性T细胞的细胞因子(如干扰素-γ)抑制细胞凋亡，而来源于2型辅助性T细胞的细胞因子(如白细胞介素4)可促进活化的单核细胞的凋亡。因此，来自单核细胞和T细胞的细胞因子调节细胞凋亡，涉及单核细胞存活中的自分泌和旁分泌调节电路。在治疗上调节单核细胞凋亡的能力有望在促进快速愈合或减少慢性炎症的免疫病理机制方面具有巨大的价值。
Apoptosis or programmed cell death is a physiological form of cell suicide that is profoundly influenced by the extracellular microenvironment. Apoptosis is characterized by a cascade of genetic and biochemical events that cause cell shrinkage, condensation of cytoplasmic and nuclear material, cleavage of chromosomal DNA into oligonucleosomesized (approximately 200 bp) fragments, and enhanced recognition of the dying cell by phagocytes. Apoptosis differs fundamentally from necrosis, the pathological form of cell death, in which the cell swells and lyses. The capacity to selectively induce apoptosis in leukocytes might be an important physiological mechanism for controlling accumulation of these cells in inflammatory lesions. In this paper, we review our data on apoptosis in human monocytes, cells which contribute both to the persistence and resolution of chronic inflammation. Apoptosis can be initiated when monocytes are cultured in the absence of appropriate exogenous stimulation. For example, addition of chemotactic factors is insufficient to block apoptosis. However, apoptosis in monocytes can be inhibited by adherence in the presence of serum, by microbial products such as lipopolysaccharide, or by certain pro-inflammatory cytokines, such as interleukin 1 and tumor necrosis factor-alpha. Cytokines derived from type 1 helper T cells (e.g., interferon-gamma) inhibit apoptosis whereas those derived from type 2 helper T cells (e.g., interleukin-4) enhance apoptosis in activated monocytes. Thus, cytokines derived from monocytes as well as T cells modulate apoptosis, implicating both autocrine and paracrine regulatory circuits in monocyte survival. The capacity to therapeutically regulate monocyte apoptosis promises to have tremendous value in promoting rapid healing or reducing the immunopathogenesis of chronic inflammation.