title: TLRs control hematopoiesis during infection.
abstract: Recent research has shown that (i) Toll-like receptor (TLR) agonists drive hematopoietic stem and progenitor cells (HSPCs) to proliferate and differentiate along the myeloid lineage in vitro, and (ii) direct TLR-mediated stimulation of HSPCs also promotes macrophage differentiation in vivo following infection. These new insights demonstrate that TLR signaling in HSPCs, in addition to other TLR-dependent mechanisms, can contribute to HSPC expansion and myeloid differentiation after infection. Evidence is, therefore, mounting that direct TLR-induced programming of hematopoiesis plays a key role in host defense by rapidly replenishing the innate immune system with the cells needed to deal with pathogens.
authors.affiliation: Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Research Division of Immunology, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
authors.forename: Alberto
authors.initials: A
authors.lastname: Yáñez
authors.forename: Helen S
authors.initials: HS
authors.lastname: Goodridge
authors.forename: Daniel
authors.initials: D
authors.lastname: Gozalbo
authors.forename: M Luisa
authors.initials: ML
authors.lastname: Gil
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D019070:Cell Lineage; D006410:Hematopoiesis / Q000276:immunology; D006412:Hematopoietic Stem Cells / Q000276:immunology*; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D007239:Infections / Q000276:immunology*; D022423:Myeloid Cells / Q000276:immunology*; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000276:immunology*
chemical_list: D051193:Toll-Like Receptors
keywords: Hematopoiesis; Hematopoietic stem and progenitor cells; Infection; TLRs