Innate Immune Memory in Hematopoietic Stem/Progenitor Cells: Myeloid-Biased Differentiation and the Role of Interferon
Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated Immune Training , in which the host animals that had experienced pathogen infection earlier acquire improved resistance to a second infection. Innate immune memory is mediated by an epigenetic m...
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| Published in | Frontiers in immunology Vol. 12; p. 621333 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Frontiers Media S.A
29.03.2021
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1664-3224 1664-3224 |
| DOI | 10.3389/fimmu.2021.621333 |
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| Abstract | Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated
Immune Training
, in which the host animals that had experienced pathogen infection earlier acquire improved resistance to a second infection. Innate immune memory is mediated by an epigenetic mechanism traced to
transcriptional memory
that is conserved throughout evolution and has been selected for the ability to mount an adaptive response to shifting environments. Accumulating evidence shows that not only peripheral myeloid cells but hematopoietic stem/progenitor cells (HSCs/HSPCs) can acquire epigenetic memory upon pathogen exposure. Systemic pathogen infection causes HSCs to exit from quiescence and facilitate myeloid-biased differentiation that leads to efficient host defense. This sequence of events is common in HSC memory generation, which is triggered by different stimuli. Recent studies show that not only pathogens but other stimuli such as metabolic stress can generate memory in HSCs. This review summarizes recent publications relevant to HSC memory. We discuss the current understanding of initial sensors, soluble mediators/cytokines involved in memory formation, including Type I and Type II interferons along with future implications. |
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| AbstractList | Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated
Immune Training
, in which the host animals that had experienced pathogen infection earlier acquire improved resistance to a second infection. Innate immune memory is mediated by an epigenetic mechanism traced to
transcriptional memory
that is conserved throughout evolution and has been selected for the ability to mount an adaptive response to shifting environments. Accumulating evidence shows that not only peripheral myeloid cells but hematopoietic stem/progenitor cells (HSCs/HSPCs) can acquire epigenetic memory upon pathogen exposure. Systemic pathogen infection causes HSCs to exit from quiescence and facilitate myeloid-biased differentiation that leads to efficient host defense. This sequence of events is common in HSC memory generation, which is triggered by different stimuli. Recent studies show that not only pathogens but other stimuli such as metabolic stress can generate memory in HSCs. This review summarizes recent publications relevant to HSC memory. We discuss the current understanding of initial sensors, soluble mediators/cytokines involved in memory formation, including Type I and Type II interferons along with future implications. Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated Immune Training, in which the host animals that had experienced pathogen infection earlier acquire improved resistance to a second infection. Innate immune memory is mediated by an epigenetic mechanism traced to transcriptional memory that is conserved throughout evolution and has been selected for the ability to mount an adaptive response to shifting environments. Accumulating evidence shows that not only peripheral myeloid cells but hematopoietic stem/progenitor cells (HSCs/HSPCs) can acquire epigenetic memory upon pathogen exposure. Systemic pathogen infection causes HSCs to exit from quiescence and facilitate myeloid-biased differentiation that leads to efficient host defense. This sequence of events is common in HSC memory generation, which is triggered by different stimuli. Recent studies show that not only pathogens but other stimuli such as metabolic stress can generate memory in HSCs. This review summarizes recent publications relevant to HSC memory. We discuss the current understanding of initial sensors, soluble mediators/cytokines involved in memory formation, including Type I and Type II interferons along with future implications.Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated Immune Training, in which the host animals that had experienced pathogen infection earlier acquire improved resistance to a second infection. Innate immune memory is mediated by an epigenetic mechanism traced to transcriptional memory that is conserved throughout evolution and has been selected for the ability to mount an adaptive response to shifting environments. Accumulating evidence shows that not only peripheral myeloid cells but hematopoietic stem/progenitor cells (HSCs/HSPCs) can acquire epigenetic memory upon pathogen exposure. Systemic pathogen infection causes HSCs to exit from quiescence and facilitate myeloid-biased differentiation that leads to efficient host defense. This sequence of events is common in HSC memory generation, which is triggered by different stimuli. Recent studies show that not only pathogens but other stimuli such as metabolic stress can generate memory in HSCs. This review summarizes recent publications relevant to HSC memory. We discuss the current understanding of initial sensors, soluble mediators/cytokines involved in memory formation, including Type I and Type II interferons along with future implications. Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated , in which the host animals that had experienced pathogen infection earlier acquire improved resistance to a second infection. Innate immune memory is mediated by an epigenetic mechanism traced to that is conserved throughout evolution and has been selected for the ability to mount an adaptive response to shifting environments. Accumulating evidence shows that not only peripheral myeloid cells but hematopoietic stem/progenitor cells (HSCs/HSPCs) can acquire epigenetic memory upon pathogen exposure. Systemic pathogen infection causes HSCs to exit from quiescence and facilitate myeloid-biased differentiation that leads to efficient host defense. This sequence of events is common in HSC memory generation, which is triggered by different stimuli. Recent studies show that not only pathogens but other stimuli such as metabolic stress can generate memory in HSCs. This review summarizes recent publications relevant to HSC memory. We discuss the current understanding of initial sensors, soluble mediators/cytokines involved in memory formation, including Type I and Type II interferons along with future implications. Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated Immune Training, in which the host animals that had experienced pathogen infection earlier acquire improved resistance to a second infection. Innate immune memory is mediated by an epigenetic mechanism traced to transcriptional memory that is conserved throughout evolution and has been selected for the ability to mount an adaptive response to shifting environments. Accumulating evidence shows that not only peripheral myeloid cells but hematopoietic stem/progenitor cells (HSCs/HSPCs) can acquire epigenetic memory upon pathogen exposure. Systemic pathogen infection causes HSCs to exit from quiescence and facilitate myeloid-biased differentiation that leads to efficient host defense. This sequence of events is common in HSC memory generation, which is triggered by different stimuli. Recent studies show that not only pathogens but other stimuli such as metabolic stress can generate memory in HSCs. This review summarizes recent publications relevant to HSC memory. We discuss the current understanding of initial sensors, soluble mediators/cytokines involved in memory formation, including Type I and Type II interferons along with future implications. |
| Author | Chen, Lili Ozato, Keiko |
| AuthorAffiliation | Division of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health , Bethesda, MD , United States |
| AuthorAffiliation_xml | – name: Division of Developmental Biology, National Institute of Child Health and Human Development, National Institutes of Health , Bethesda, MD , United States |
| Author_xml | – sequence: 1 givenname: Lili surname: Chen fullname: Chen, Lili – sequence: 2 givenname: Keiko surname: Ozato fullname: Ozato, Keiko |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33854500$$D View this record in MEDLINE/PubMed |
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| Keywords | HSC interferon trained immunity myeloid-bias epigenetic memory |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Present address: Lili Chen, Center for Stem Cell and Regenerative Disease, Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (IMM), The University of Texas Health Science Center at Houston, Houston, TX, United States Edited by: Jose Luis Subiza, Inmunotek SL, Spain This article was submitted to Vaccines and Molecular Therapeutics, a section of the journal Frontiers in Immunology Reviewed by: Hitoshi Takizawa, Kumamoto University, Japan; Maziar Divangahi, McGill University, Canada |
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| Snippet | Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated
Immune Training
, in which the host animals that had... Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated , in which the host animals that had experienced... Innate immune memory was first described for monocytes and other myeloid cells. This memory is designated Immune Training, in which the host animals that had... |
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| SubjectTerms | Animals Cell Differentiation Cells, Cultured Epigenesis, Genetic epigenetic memory Hematopoietic Stem Cells - physiology HSC Humans Immunity, Innate Immunologic Memory Immunology interferon Interferons - metabolism Mice Myeloid Cells - physiology myeloid-bias trained immunity |
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| Title | Innate Immune Memory in Hematopoietic Stem/Progenitor Cells: Myeloid-Biased Differentiation and the Role of Interferon |
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