Table 1.

Cytokines, growth factors, and pathways/transcription factors involved in HSC function and their different inflammatory sources

Growth factor/inflammatory cytokine	Sources of inflammation	Main effects on HSCs	Pathways/transcription factors in HSCs
G-CSF	Bacterial infections, cancer, autoimmune disease [58]	Emergency granulopoiesis [118], proliferation [119], mobilization [120]	G-CSFR-STAT3-C/EBP ß [77, 118], C/EBPα [121]
			SOCS3 (negative regulator) [122]
GM-CSF and M-CSF	Bacterial infections, cancer	Emergency granulopoiesis [121], extramedullary myelopoiesis [123], trained immunity [124], monocyte differentiation [125]	G-CSFR [126]
			PU.1 [125]
IFN type II	Acute and chronic bacterial and virus infections (mycobacteria [7••, 8•], LCMV [127]), fungi infections [53], clonal hematopoiesis [128], aplastic anemia [129], liver cirrhosis [130], HLH disorder [131, 132], cancer [133], autoimmune disease [58]	Proliferation [7••, 127], impaired self-renewal capacity, secondary stress-induced apoptosis [8•], myeloid differentiation [9], trained immunity [134]	IFNG receptors and Stat1 [7••]
			Batf2 in terminal differentiation [8•]
IFN type I	Bacterial [21] viral infections, fungi infections [53], cancer, DNA-stimulated cell death [135]	Proliferation (short term), impaired HSC repopulation capacity (long term) [136], impairment and attrition [137], apoptosis [21], stimulate proliferation and post-transcriptional protein synthesis in a primed subpopulation of stem cell–like megakaryocyte-committed progenitor [138]	IFN-α/ß receptor and STAT1 [136]
			IRF2 (negative regulator) [139], IRF3 [140]
			Reduction expression involved in cell quiescence (p27, p57, Foxo1, Foxo3, Pten) [141]
			ROS-production in DNA damage [137]
			NFAT5 (negative regulator) [140]
LPS	Gram-negative bacterial infections (i.e., E. coli, Salmonella [4•, 14•])	Proliferation, migration [4•], myeloid skewing and halter engraftment capacity [14•], extramedullary hematopoiesis [14•], trained immunity [142]	TLR4 [14•], NOD1/2, Myd88-TRIF-ROS-p38 [4•]
			RIPK2- NF-κB-MAPK [143]
			C/EBP ß [142]
TNFα	Bacterial infections, cancer, aging [72], liver cirrhosis [130], autoimmune disease [58], aging [73, 74], neurological disorder [63]	Proliferation, myeloid differentiation, and repopulation capacity [144]. Self-renewal, resistance to TNFα-derived apoptosis	TNFα production required for PU.1 induction by LPS [145], NFKb, CXCR4, HDAC5
IL-1	Bacterial infections, cancer [146], wounds [23], DNA-stimulated cell death [135], aging [72], liver cirrhosis [130], autoimmune disease [58, 147], neurological disorder	Proliferation, myeloid differentiation, impaired self-renew (chronic administration) [148], local granulopoiesis [23], trained immunity [124]	IL-1R-NF-κB-PU.1 [148]
IL-6	Bacterial infections, cancer, aging [71, 72], neurological disorder [63, 64], microbiota [149]	Proliferation and myeloid differentiation [150]	Shp2/Stat3/Morbid [151]