Our immune system has to cope with a variety of pathogens, demanding the ability to dynamically respond to adverse conditions. Stress hematopoiesis is induced when the need for new blood and immune cells exceeds their steady-state production. Reduced levels of Red Blood Cells (RBCs) or platelets, as well as various immune stimuli, can call for urgent hematopoiesis. As blood system function is closely tied to overall physiological health and impaired function can predispose individuals toward disease, the dynamics and possible consequences of stress hematopoiesis have become a topic of significant scientific and clinical interest.
Hematopoietic Stem Cells (HSCs) can be activated rapidly following immune-stimulation in vivo, setting the system ready for accelerated production of needed blood cell lineages. HSCs are the multipotent self-renewing source for all blood and immune cells. They are mostly quiescent in the bone-marrow at steady-state and may become activated. Indeed, major mediators such as interferons or other inflammatory cytokines are known to directly activate HSCs, demonstrating that immune responses can call for emergency actions of the bone marrow. Recent studies using advanced molecular and functional profiling have revealed mechanisms that activate HSC proliferation and differentiation in response to acute infection or chronic immune stimulation.
The study of inflammation-induced stress-hematopoiesis gained major advancements over the last years, yet much remains to be explored and understood. We humans continuously experience immunological challenges, some minor and transient, others can be severe and/or chronic. Is the difference quantitative or is there a qualitative step between different levels of stress? Aging is also known to change hematopoiesis, however little is understood why hallmarks of HSC-aging are shared with stressed-hematopoiesis. Is there one underlying mechanism, a coincidence of phenotypic-similarity, or convergence of unrelated phenomena? Discoveries of mediating factors are suggesting direct ways to study inflammation-induced stress-hematopoiesis and develop clinical interventions. The acute activation of HSCs from deep quiescence into proliferation has a possible toll, genetically and epigenetically. HSCs do remember, and we better learn how to get through inevitable stress without carrying long-term impairments, both for the stem cells as well as in the downstream immune system.
This Research Topic aims at highlighting major innovations in experimental hematology that have defined the connections between immunological perturbations and HSCs. We encourage authors to submit Original Research and Reviews focused on, but not limited to, the following topics:
1. Impact of inflammatory cytokines on HSCs
2. Bone marrow niche under inflammation
3. Specific pathogenic infections that affect HSCs
4. Short- and Long-term changes in HSCs following immune stimulation
5. Immune effector cells that regulate HSCs
Our immune system has to cope with a variety of pathogens, demanding the ability to dynamically respond to adverse conditions. Stress hematopoiesis is induced when the need for new blood and immune cells exceeds their steady-state production. Reduced levels of Red Blood Cells (RBCs) or platelets, as well as various immune stimuli, can call for urgent hematopoiesis. As blood system function is closely tied to overall physiological health and impaired function can predispose individuals toward disease, the dynamics and possible consequences of stress hematopoiesis have become a topic of significant scientific and clinical interest.
Hematopoietic Stem Cells (HSCs) can be activated rapidly following immune-stimulation in vivo, setting the system ready for accelerated production of needed blood cell lineages. HSCs are the multipotent self-renewing source for all blood and immune cells. They are mostly quiescent in the bone-marrow at steady-state and may become activated. Indeed, major mediators such as interferons or other inflammatory cytokines are known to directly activate HSCs, demonstrating that immune responses can call for emergency actions of the bone marrow. Recent studies using advanced molecular and functional profiling have revealed mechanisms that activate HSC proliferation and differentiation in response to acute infection or chronic immune stimulation.
The study of inflammation-induced stress-hematopoiesis gained major advancements over the last years, yet much remains to be explored and understood. We humans continuously experience immunological challenges, some minor and transient, others can be severe and/or chronic. Is the difference quantitative or is there a qualitative step between different levels of stress? Aging is also known to change hematopoiesis, however little is understood why hallmarks of HSC-aging are shared with stressed-hematopoiesis. Is there one underlying mechanism, a coincidence of phenotypic-similarity, or convergence of unrelated phenomena? Discoveries of mediating factors are suggesting direct ways to study inflammation-induced stress-hematopoiesis and develop clinical interventions. The acute activation of HSCs from deep quiescence into proliferation has a possible toll, genetically and epigenetically. HSCs do remember, and we better learn how to get through inevitable stress without carrying long-term impairments, both for the stem cells as well as in the downstream immune system.
This Research Topic aims at highlighting major innovations in experimental hematology that have defined the connections between immunological perturbations and HSCs. We encourage authors to submit Original Research and Reviews focused on, but not limited to, the following topics:
1. Impact of inflammatory cytokines on HSCs
2. Bone marrow niche under inflammation
3. Specific pathogenic infections that affect HSCs
4. Short- and Long-term changes in HSCs following immune stimulation
5. Immune effector cells that regulate HSCs
