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Table 2 Characterization of myeloid cell subsets

From: Immune cell subset differentiation and tissue inflammation

Subsets   Markers Frequency Cytokines Functions
DC cDC CD11c+MHCII+CD141+(BDCA3+)XCR1+CLEC9A+FLT3+CD103+ 5~10% in blood IL-12, IFN-III ↑IFN-IIICross-present Ag
CD11c+MHCII+(BDCA1+)CD172a+CD11b+FLT3+ 45–50% in blood IL-23? Present Ag
pDC BDCA2+LILRA4+CD45RA+ 45–50% in blood IFNα Sense pathogenActivate IC
mDC MHCII+CD11c+CD86+CD40+CD80+CD83+CCR7+CD14 Induced by inflammation TNFα, iNOSIL-12, IL-23 Cross-present Ag
MC Classical CD14+CD16CXCR1+ CXCR2+CD62L+ 80–95% in MNC ROS, NO, MPOIFN-I, IL-1α, TNFIL-6, IL-8, CCL2 Phagocytosis↑Inflammation
Intermediate CD14+CD16+CD64intCCR1intCCR2int CX3CR1int CD11bint CD33int CD115int CD40+ CD54+ HLA-DR+ 2–11% in MNC ROS, NO, MPOIFN-I, IL-1α, TNFIL-6, IL-8 CCL2 ↑Inflammation
Non-classical CD14CD16+ 2–8% in MNC TNF, IL-1β, CCL3 Patrol, repair tissue
CD40 CD14+CD40+ 64% in PBMC TNFα, IL-6 ↑Inflammation
M1 iNOS+CXCL11+IL-12high IL-23highIL-10low 1% in gastric tissue IL-6, TNFαiNOS, IL-12 Microbicidal↑Inflammation
M2a FIZZ1+Arg1+IL-12lowIL-23low 1% in gastric tissue IL-10 ↓InflammationHeal woundRepair tissue
M2b CD80highCD14highHLA-DRlowIL-12lowIL-23low 0 in PBMC IL-10 Activate Th2↓Inflammation
M2c CD86lowHLA-DRlowCD163+TLR4highIL-12lowIL-23low 2.4% in CD68+ CCL18 ↓InflammationDeposit matrixRemodel tissue
M4 MMP7+MR+S100A8+CD68+ 31.7% in CD68+ MØ from coronary artery CD86, IL-6, TNFα ↑Inflammation
Mhem HOMX1+CD163+ 25% in thrombosis IL-10 ↓Lipid accumulationRetain iron, ↓Inflammation
  1. Four kinds of dendritic cells (DC) can be defined in human based in part on their functional specialization: monocyte-derived DC (mDC), CD103+ classical/conventional dendritic cell (cDC), CD11b + cDC, and plasmocytoid dendritic cell (pDC). mDC exhibit a strong costimulatory capacity for TC activation. cDC are the most efficient cell type for priming and functional polarization of TC. pDCs can secrete high concentrations of interferon (IFN)-I (mainly IFN-α). In humans, there are three populations of monocytes (MC), as defined by the expression of CD14 and CD16 (CD14++CD16−, CD14+CD16+, and CD14+CD16++). The CD14++CD16− MC represent 80% to 90% of blood MC, express high levels of the chemokine receptor C-C chemokine receptor type 2 (CCR2) and low levels of CX3C chemokine receptor 1 (CX3CR1), and produce IL-10 rather than TNF and IL-1 in response to lipopolysaccharide (LPS) in vitro. CD14+CD16+ MC express the Fc receptors CD64 and CD32, have phagocytic activity, and are entirely responsible for the production of tumor necrosis factor-α (TNF-α) and IL-1 in response to LPS. In contrast, CD14+CD16++ MC lack the expression of other Fc receptors, are poorly phagocytic, and do not produce TNF-α or IL-1 in response to LPS. Our lab recently identified CD40+ MC as a stronger inflammatory subset related to chronic kidney disease (CKD). Macrophages (MØ) also display phenotypic heterogeneity. Depending on the stimuli, M0 MØ could polarize towards the pro-inflammatory M1 subset by lipopolysaccharide or IFN-γ, or towards the alternative M2a type by IL-4. M2b MØs are induced upon combined exposure to immune complexes and Toll-like receptor (TLR) ligands or IL-1 receptor agonists. M2c MØs are induced by IL-10 and glucocorticoids. Atheroprotective Mhem subset could be induced by hemoglobin, and highly express haem oxygenase 1 and CD163. Chemokine (C-X-C motif) ligand 4 drives differentiation of human specific M4 MØ, with unique expression of surface markers such as S100A8, mannose receptor CD206, and matrix metalloproteinase 7