A subpopulation of human bone marrow erythroid cells displays a myeloid gene expression signature similar to that of classic monocytes.
Roman Perik-ZavodskiiOlga Perik-ZavodskaiaJulia ShevchenkoMarina VolynetsSaleh AlrhmounKirill NazarovVera DenisovaSergey SennikovPublished in: PloS one (2024)
Erythroid cells, serving as progenitors and precursors to erythrocytes responsible for oxygen transport, were shown to exhibit an immunosuppressive and immunoregulatory phenotype. Previous investigations from our research group have revealed an antimicrobial gene expression profile within murine bone marrow erythroid cells which suggested a role for erythroid cells in innate immunity. In the present study, we focused on elucidating the characteristics of human bone marrow erythroid cells through comprehensive analyses, including NanoString gene expression profiling utilizing the Immune Response V2 panel, a BioPlex examination of chemokine and TGF-beta family proteins secretion, and analysis of publicly available single-cell RNA-seq data. Our findings demonstrate that an erythroid cell subpopulation manifests a myeloid-like gene expression signature comprised of antibacterial immunity and neutrophil chemotaxis genes which suggests an involvement of human erythroid cells in the innate immunity. Furthermore, we found that human erythroid cells secreted CCL22, CCL24, CXCL5, CXCL8, and MIF chemokines. The ability of human erythroid cells to express these chemokines might facilitate the restriction of immune cells in the bone marrow under normal conditions or contribute to the ability of erythroid cells to induce local immunosuppression by recruiting immune cells in their immediate vicinity in case of extramedullary hematopoiesis.
Keyphrases
- induced apoptosis
- bone marrow
- cell cycle arrest
- single cell
- gene expression
- rna seq
- endothelial cells
- immune response
- endoplasmic reticulum stress
- mesenchymal stem cells
- stem cells
- dna methylation
- oxidative stress
- cell death
- signaling pathway
- dendritic cells
- toll like receptor
- machine learning
- cell proliferation
- staphylococcus aureus
- acute myeloid leukemia
- high throughput
- epithelial mesenchymal transition
- induced pluripotent stem cells
- transcription factor
- liver fibrosis