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Toll-like receptor signaling in hematopoietic stem and progenitor cells

Capitano, Maegan L.

Current Opinion in Hematology: July 2019 - Volume 26 - Issue 4 - p 207–213
doi: 10.1097/MOH.0000000000000511
HEMATOPOIESIS: Edited by Hal E. Broxmeyer and Maegan L. Capitano

Purpose of review The innate immune system is essential in the protection against microbial infection and facilitating tissue repair mechanisms. During these stresses, the maintenance of innate immune cell numbers through stress-induced or emergency hematopoiesis is key for our survival. One major mechanism to recognize danger signals is through the activation of Toll-like receptors (TLRs) on the surface of hematopoietic cells, including hematopoietic stem cell (HSC) and hematopoietic progenitor cell (HPC), and nonhematopoietic cells, which recognize pathogen-derived or damaged-induced compounds and can influence the emergency hematopoietic response. This review explores how direct pathogen-sensing by HSC/HPC regulates hematopoiesis, and the positive and negative consequences of these signals.

Recent findings Recent studies have highlighted new roles for TLRs in regulating HSC and HPC differentiation to innate immune cells of both myeloid and lymphoid origin and augmenting HSC and HPC migration capabilities. Most interestingly, new insights as to how acute versus chronic stimulation of TLR signaling regulates HSC and HPC function has been explored.

Summary Recent evidence suggests that TLRs may play an important role in many inflammation-associated diseases. This suggests a possible use for TLR agonists or antagonists as potential therapeutics. Understanding the direct effects of TLR signaling by HSC and HPC may help regulate inflammatory/danger signal-driven emergency hematopoiesis.

Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA

Correspondence to Maegan L. Capitano, PhD, Department of Microbiology and Immunology, Indiana University School of Medicine, R2 Room 312, 950 West Walnut Street, Indianapolis, IN 46202, USA. Tel: +1 317 274 7555; fax: +1 317 274 7592; e-mail:

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