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Cited by 62

The DOI matches its Crossref record; 182 of the 182 references it cites were found in a registry or an index.

Stress and Non-Stress Roles of Inflammatory Signals during HSC Emergence and Maintenance

Clapes, Thomas, Lefkopoulos, Stylianos, Trompouki, Eirini·2016·Frontiers in Immunology
DOI 10.3389/fimmu.2016.00487PMC PMC5098161
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Abstract

Hematopoietic stem cells (HSCs) are a rare population that gives rise to almost all cells of the hematopoietic system, including immune cells. Until recently, it was thought that immune cells sense inflammatory signaling and HSCs respond only secondarily to these signals. However, it was later shown that adult HSCs could directly sense and respond to inflammatory signals, resulting in a higher output of immune cells. Recent studies demonstrated that inflammatory signaling is also vital for HSC ontogeny. These signals are thought to arise in the absence of pathogens, are active during development, and indispensable for HSC formation. In contrast, during times of stress and disease, inflammatory responses can be activated and can have devastating effects on HSCs. In this review, we summarize the current knowledge about inflammatory signaling in HSC development and maintenance, as well as the endogenous molecular cues that can trigger inflammatory pathway activation. Finally, we comment of the role of inflammatory signaling in hematopoietic diseases.

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Figure 1 Inflammatory signaling is required for HSC emergence. Left panel: HSC specification in zebrafish embryos. Neutrophils produce TNFα that binds Tnfr2, expressed by endothelial cells (EC). Activation of Tnfr2 leads to upregulation of jag1a and activation of Notch signaling in the hemogenic endothelium (HE), ultimately leading to the activation of NF-κB. Alternatively, Tlr4/Myd88 also induce NF-κB, crucial for HSC specification throughout endothelial-to-hematopoietic transition. Downstream of Notch1 activation, Ifng participates in HSC specification in a cell autonomous fashion. IL-1β signaling, downstream of the TLR4–MyD88–NF-κB axis has also an impact on HSC emergence as does Ifn-ϕ. Finally, Gcsf acts on newly generated HSCs and contributes to HSC proliferation; however, the mechanism is still unclear. Right panel: HSC specification in mouse embryos. Contrary to zebrafish embryos, it is still unclear how inflammatory pathways are being regulated in the developing embryo, or what are the sources of inflammatory cytokines. Nevertheless, it is clear that IFN-α, IFN-γ, as well as Il-1β, IL-3, and TLR4 are required for proper HSC specification, possibly engaging Notch1 signaling and Runx1 and/or NF-κB.
Figure 1 Inflammatory signaling is required for HSC emergence. Left panel: HSC specification in zebrafish embryos. Neutrophils produce TNFα that binds Tnfr2, expressed by endothelial cells (EC). Activation of Tnfr2 leads to upregulation of jag1a and activation of Notch signaling in the hemogenic endothelium (HE), ultimately leading to the activation of NF-κB. Alternatively, Tlr4/Myd88 also induce NF-κB, crucial for HSC specification throughout endothelial-to-hematopoietic transition. Downstream of Notch1 activation, Ifng participates in HSC specification in a cell autonomous fashion. IL-1β signaling, downstream of the TLR4–MyD88–NF-κB axis has also an impact on HSC emergence as does Ifn-ϕ. Finally, Gcsf acts on newly generated HSCs and contributes to HSC proliferation; however, the mechanism is still unclear. Right panel: HSC specification in mouse embryos. Contrary to zebrafish embryos, it is still unclear how inflammatory pathways are being regulated in the developing embryo, or what are the sources of inflammatory cytokines. Nevertheless, it is clear that IFN-α, IFN-γ, as well as Il-1β, IL-3, and TLR4 are required for proper HSC specification, possibly engaging Notch1 signaling and Runx1 and/or NF-κB.CC BY · PubMed Central

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Metadata

Authors
Clapes, T., Lefkopoulos, S., & Trompouki, E.
Venue
Frontiers in Immunology
Publisher
Frontiers Media SA
Published
2016-11-07
Volume
7
ISSN
1664-3224
DOI
10.3389/fimmu.2016.00487
PMC
PMC5098161
Cited by
62
References
182

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