Chronic immune response dysregulation in MDS pathogenesis
Open accessAbstract
Chronic innate immune signaling in hematopoietic cells is widely described in myelodysplastic syndromes (MDS), and innate immune pathway activation, predominantly via pattern recognition receptors, increases the risk of developing MDS. An inflammatory component to MDS has been reported for many years, but only recently has evidence supported a more direct role of chronic innate immune signaling and associated inflammatory pathways in the pathogenesis of MDS. Here we review recent findings and discuss relevant questions related to chronic immune response dysregulation in MDS.
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Human MDS HSPCs show significant innate immune system dysregulation and resistance to the pro-proliferative effects of inflammation.
“Human myelodysplastic syndrome (MDS) HSPCs have shown significant innate immune system dysregulation and resistance to the pro-proliferative effects of inflammation [69,80,81].”
From Clonal hematopoiesis and inflammation – the perpetual cycle (2023) · cites this paper as [80]
The section “Expression of immune-related genes in MDS hematopoietic stem/progenitor cells” says innate immune-related gene dysregulation is common in MDS HSPCs. The cited paper does not establish that MDS HSPCs resist inflammation’s pro-proliferative effects; its “Activation of immune receptors in MDS” section instead describes increased proliferation after TLR stimulation in human HSPCs generally, without specifying MDS HSPCs. (LLM, conf=0.84)
Experimental — accuracy not yet measuredDysregulated inflammatory signaling has emerged as a key partner alongside oncogenic mutations in the development and/or progression of hematological malignancy.
“Dysregulated inflammatory signaling has emerged as a key partner alongside oncogenic mutations in the development and/or progression of hematological malignancy (Barreyro et al., 2018; Pietras, 2017).”
From PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress (2021) · cites this paper as Barreyro et al., 2018
The Introduction and Conclusions identify chronic innate immune signaling as a contributor to MDS pathogenesis, and the section on innate immune signaling and clonal hematopoiesis describes proposed routes linking inflammatory signaling and somatic mutations. The paper focuses on MDS rather than hematological malignancies generally, and its Conclusions leave how immune signaling cooperates with genetic defects as an open question. (LLM, conf=0.85)
Experimental — accuracy not yet measuredChronic inflammation, often associated with increased IL-1 activity, is a common phenotype in individuals at risk for hematological malignancy, which can be related to several preexisting factors, including aging/tissue decline, genotoxin exposure, metabolic dysfunction, and/or autoimmune disease.
“Chronic inflammation, often associated with increased IL-1 activity, is a common phenotype in individuals at risk for hematological malignancy, which can be related to several preexisting factors, including aging/tissue decline, genotoxin exposure, metabolic dysfunction, and/or autoimmune disease (Barreyro et al., 2018; Pietras, 2017).”
From PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress (2021) · cites this paper as Barreyro et al., 2018
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“This includes myeloid malignancies like myelodysplastic syndrome (MDS) (Ganan-Gomez et al., 2015; Zambetti et al., 2016; Barreyro et al., 2018; Trowbridge and Starczynowski, 2021) and acute myelogenous leukemia (AML) (Carey et al., 2017; Chakraborty et al., 2021).”
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- Authors
- Barreyro, L., Chlon, T. M., & Starczynowski, D. T.
- Affiliations
- Cincinnati Children's Hospital Medical Center (US)
- Corresponding author
- Barreyro, Laura
- Chlon, Timothy M.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2018-10-11
- Volume
- 132
- Issue
- 15
- Pages
- 1553-1560
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC6182269
- OpenAlex
- W2885816375
- Cited by
- 226
- References
- 114
- Citations by year
- 2026: 16 · 2025: 31 · 2024: 28 · 2023: 26 · 2022: 43 · 2021: 35 · 2020: 23 · 2019: 23 · 2018: 1
- FWCI
- 3.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Society of Hematology
- Leukemia and Lymphoma Society
- Cincinnati Children's Hospital Medical Center
- National Institutes of Health (1f32hl143993-01, RO1DK102759)
- National Heart, Lung, and Blood Institute (R35HL135787, F32 HL143993)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK102759, RO1DK102759, R01DK113639)
- National Institute of Environmental Health Sciences (T32ES007250)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
- Keywords
- myelodysplastic syndrome, innate immune signaling, pattern recognition receptors, inflammation, hematopoietic cells, MDS pathogenesis
- MeSH terms
- Animals, Hematopoietic Stem Cells, Humans, Immunity, Innate, Inflammation, Myelodysplastic Syndromes
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