Abstract
Lifelong, self-renewing, and, multilineage-differentiating hematopoietic stem cells (HSCs) gradually divide in steady-state bone marrow (BM). Conversely, in cases of hematopoietic stress, including infection and inflammation, hematopoiesis is highly demanded due to massive cell consumption in the stressed tissues and involves HSC recruitment to fulfil the hematopoietic demand. Accumulating evidence indicates that infection-related inflammation acts on blood-forming HSCs and progenitors within the BM to facilitate hematopoiesis for self-defense. In this review, we discuss the mechanisms used by various inflammatory responses involving not only HSCs but also the niche cells in the BM, a site that has long been considered an immune-privileged organ.
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