Common Sources of Inflammation and Their Impact on Hematopoietic Stem Cell Biology

Author:

Hormaechea-Agulla Daniel,Le Duy T.,King Katherine Y.

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology,Developmental Biology,Genetics,Molecular Biology

Reference151 articles.

1. •• King KY, Goodell MA. Inflammatory modulation of HSCs: viewing the HSC as a foundation for the immune response. Nat Rev Immunol. 2011;11(10):685–92. This review summarizes the effects of infection on hematopoietic stem cell function and how these effects may have a pivotal role in directing the immune response from the bone marrow.

2. •• Chavakis T, Mitroulis I, Hajishengallis G. Hematopoietic progenitor cells as integrative hubs for adaptation to and fine-tuning of inflammation. Nat Immunol. 2019;20(7):802–11. This review discusses the mechanisms that govern the adaptation of hematopoietic progenitor cells to inflammation and its sequelae in the pathogenesis of human disease.

3. • Kovtonyuk LV, et al. Inflamm-aging of hematopoiesis, hematopoietic stem cells, and the bone marrow microenvironment. Front Immunol. 2016;7:502. This comprehensive review present evidence supporting the concept of “Inflamm-Aging,” or inflammation-associated aging of hematopoiesis and their effects on bone marrow microenvironment.

4. • Takizawa H, et al. Pathogen-induced TLR4-TRIF innate immune signaling in hematopoietic stem cells promotes proliferation but reduces competitive fitness. Cell Stem Cell. 2017;21(2):225–40 e5. This study shows that while direct TLR4 activation in HSCs might be beneficial for controlling systemic infection, prolonged TLR4 signaling has detrimental effects and may contribute to inflammation-associated HSPC dysfunction.

5. • Boettcher S, et al. Endothelial cells translate pathogen signals into G-CSF-driven emergency granulopoiesis. Blood. 2014;124(9):1393–403. This elegant study shows that endothelial cells (ECs), but not hematopoietic cells, hepatocytes, pericytes, or BM stromal cells, are essential cells for emergency granulopoiesis driven by G-CSF.

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