Askenasy Nadir
Frankel Laboratory, Schneider Children's Medical Center of Israel, Petach Tikva 49202, Israel.
Blood Rev. 2015 Jan;29(1):11-5. doi: 10.1016/j.blre.2014.09.002. Epub 2014 Sep 16.
Enhanced hematopoiesis accompanies systemic responses to injury and infection. Tumor necrosis factor (TNF) produced by injured cells and interferons (IFNs) secreted by inflammatory cells is a co-product of the process of clearance of debris and removal of still viable but dysfunctional cells. Concomitantly, these cytokines induce hematopoietic stem and progenitor cell (HSPC) activity as an intrinsic component of the systemic response. The proposed scenario includes induction of HSPC activity by type I (IFNα/β) and II (IFNγ) receptors within the quiescent bone marrow niches rendering progenitors responsive to additional signals. TNFα converges as a non-selective stimulant of HSPC activity and both cytokines synergize with other growth factors in promoting differentiation. These physiological signaling pathways of stress hematopoiesis occur quite frequent and do not cause HSPC extinction. The proposed role of IFNs and TNFs in stress hematopoiesis commends revision of their alleged involvement in bone marrow failure syndromes.
增强的造血作用伴随着机体对损伤和感染的全身性反应。受损细胞产生的肿瘤坏死因子（TNF）以及炎性细胞分泌的干扰素（IFN）是清除碎片和清除仍存活但功能失调细胞过程的共同产物。同时，这些细胞因子诱导造血干细胞和祖细胞（HSPC）的活性，作为全身反应的内在组成部分。提出的设想包括静止骨髓龛内的I型（IFNα/β）和II型（IFNγ）受体诱导HSPC活性，使祖细胞对其他信号作出反应。TNFα作为HSPC活性的非选择性刺激物发挥作用，并且这两种细胞因子在促进分化方面与其他生长因子协同作用。应激造血的这些生理信号通路相当频繁地发生，并且不会导致HSPC耗竭。IFN和TNF在应激造血中的假定作用值得重新审视它们在骨髓衰竭综合征中所谓的参与情况。
