Microbiota-driven immune signaling pathways and their effects on the hematopoietic system
| Microbiome-driven signaling pathway . | Effects on hematopoietic system . | Reference . |
|---|---|---|
| NOD1 signaling | Promotes steady-state hematopoiesis indirectly through the induction of cytokines by mesenchymal stromal cells | 42 |
| RAC1-NOD1-RIPK2-NF-κB axis initiates inflammatory signaling in the HE, resulting in HSPC specification | 25 | |
| NOD1 signaling in hematopoietic compartment regulates proinflammatory macrophage polarization and neutrophil infiltration in adipose tissue | 22 | |
| TLR-MYD88 signaling | Bacterial recognition during infection promotes the G-CSF secretion from endothelial cells and monocytes, leading to the acceleration of granulopoiesis | 23 |
| TLR4 signaling promotes B-cell maturation | 43 | |
| Toll-like receptor activation in human monocytes induces rapid differentiation DC-SIGN+CD16+ macrophages and CD1b+DC-SIGN− dendritic cells | 44 | |
| TLR7 stimulation at epithelial surfaces drives emergency myelopoiesis | 29 | |
| TLR2 activation results in HSC expansion in both the BM and spleen, increased HSC cycling, and a reduction in BM megakaryocyte-erythroid progenitors | 31 | |
| RIG-I MAVS signaling | Controls the emergence of hematopoietic precursors in zebrafish embryos through downstream IFN signaling | 33 |
| Activation of RIG-1 by repetitive element RNA, expressed during the endothelial-to-hematopoietic transition modulates the inflammatory signaling ie, crucial for HSPC formation during development | 34 | |
| cGAS-STING signaling | cia-cGAS is a suppressor of cGAS. deficiency of cia-cGAS promotes STING activation leading to increased HSC cycling and cGAS-mediated HSC exhaustion | 45 |
| Excessive R-loop accumulation because of DDX41 insufficiency, results in cGAS-STING-NF-κB pathway activation to promote HSPC expansion | 35 | |
| Activation of STING pathway by bacterial c-di-GMP activates in a cGAS-independent manner, induces HSPC proliferation, and mobilization as well as myeloid-biased differentiation, but reduces HSC self-renewal and mobilization | 46 |
| Microbiome-driven signaling pathway . | Effects on hematopoietic system . | Reference . |
|---|---|---|
| NOD1 signaling | Promotes steady-state hematopoiesis indirectly through the induction of cytokines by mesenchymal stromal cells | 42 |
| RAC1-NOD1-RIPK2-NF-κB axis initiates inflammatory signaling in the HE, resulting in HSPC specification | 25 | |
| NOD1 signaling in hematopoietic compartment regulates proinflammatory macrophage polarization and neutrophil infiltration in adipose tissue | 22 | |
| TLR-MYD88 signaling | Bacterial recognition during infection promotes the G-CSF secretion from endothelial cells and monocytes, leading to the acceleration of granulopoiesis | 23 |
| TLR4 signaling promotes B-cell maturation | 43 | |
| Toll-like receptor activation in human monocytes induces rapid differentiation DC-SIGN+CD16+ macrophages and CD1b+DC-SIGN− dendritic cells | 44 | |
| TLR7 stimulation at epithelial surfaces drives emergency myelopoiesis | 29 | |
| TLR2 activation results in HSC expansion in both the BM and spleen, increased HSC cycling, and a reduction in BM megakaryocyte-erythroid progenitors | 31 | |
| RIG-I MAVS signaling | Controls the emergence of hematopoietic precursors in zebrafish embryos through downstream IFN signaling | 33 |
| Activation of RIG-1 by repetitive element RNA, expressed during the endothelial-to-hematopoietic transition modulates the inflammatory signaling ie, crucial for HSPC formation during development | 34 | |
| cGAS-STING signaling | cia-cGAS is a suppressor of cGAS. deficiency of cia-cGAS promotes STING activation leading to increased HSC cycling and cGAS-mediated HSC exhaustion | 45 |
| Excessive R-loop accumulation because of DDX41 insufficiency, results in cGAS-STING-NF-κB pathway activation to promote HSPC expansion | 35 | |
| Activation of STING pathway by bacterial c-di-GMP activates in a cGAS-independent manner, induces HSPC proliferation, and mobilization as well as myeloid-biased differentiation, but reduces HSC self-renewal and mobilization | 46 |
cGAS, cyclic GMP-AMP synthase; GMP, guanosine monophosphate; HE, hemogenic endothelium.