Table 1.
Cell types | Development of inflammation | References | Resolution of inflammation | References | ||||||
---|---|---|---|---|---|---|---|---|---|---|
Subpopulations | Surface Markers | Active molecules | Effector activity | Subpopulations | Surface Markers | Active molecules | Effector activity | |||
Neutrophils | N1-neutrophils | CD11b | MPO | NETosis | (31, 34, 36, 37) | N2-neutrophils | CD11b | VEGF | Macrophages polarization | (31, 43, 45, 149) |
CD16 | ROS | Degranulation | CD206+ | MMP-9 | Angiogenesis | |||||
CD15 | leukotrines | Phagocytosis | ? | MMP-12 | ||||||
CD87 | ||||||||||
N1-neutrophils | CD11b | resolvins | SPM synthesis | (17, 18, 29, 31, 32, 40) | ||||||
CD16 | annexin A1 | Formation of apoptotic bodies | ||||||||
CD15 | lipocalin | |||||||||
CD87 | lactoferrin | |||||||||
cathelicidin | ||||||||||
Eosinophils | Inflammatory eosinophils? | Siglec-Fhi (mice) | ROS | EETosis | (47, 52) | Regulatory eosinophils? | Siglec-Fint (mice) | IL-4 | Macrophages polarization | (13, 49, 51, 53, 54) |
CD62L– | major basic protein | Degranulation | Siglec-8+ (humans) | TGF-β | Angiogenesis | |||||
CD49d | eosinophil cationic protein | Oxidative burst | CD62L+ | VEGF | ||||||
CD101hi | eosinophil peroxidase | CD101lo | FGF | |||||||
arachidonic acid derivatives | ? | resolvin RvE3 | ||||||||
IL-5 | protectin D1 | |||||||||
Monocytes | Classical monocytes | CD14++CD16neg/Ly-6Chi (mice) | TNF-α | Secretion of inflammatory cytokines | (12, 67) | Non-classical monocytes | CD14+CD16hi/Ly-6Clo | VEGF | Secretion of anti-inflammatory and angiogeneic cytokines | (12, 67) |
Intermediate monocytes | CD14++CD16hi | IL-1β | CXC3R1 | TGF-β | ||||||
CCR2 | IL-6 | |||||||||
TIE-2 | NO | |||||||||
Macrophages | M1-macrophages? | CD68 | IL-12 | Phagocytosis | (12, 70) | M2- macrophages (M2a, M2b, M2c)? | CD206 | IL-10 | Secretion of anti-inflammatory and angiogeneic cytokines | (72, 73, 75, 78) |
MHC II | IL-23 | Secretion of inflammatory cytokines | CD163 | IL-1Ra | ||||||
CD86 | ROS | Stabilin-1 | TGF-β | |||||||
NO | VEGF | |||||||||
leukotriens | Arginase | |||||||||
SPM (resolvins, maresins, lipoxins, protectins) | SPM synthesis | |||||||||
Efferocytosis | ||||||||||
Mast cells | MCCT | CD64 | cathepsin G | Secretion of inflammatory cytokines | (84, 87) | ? | ? | chymase | Regulation of fibrosis | (84, 90, 91) |
CD117 | carboxypeptidase | Degranulation | tryptase | |||||||
histamine | Collagen degradation | bFGF | ||||||||
TNF-α | IL-10 | |||||||||
IL-6 | IL-13 | |||||||||
IFN-γ | VEGF-A | |||||||||
Dendritic cells | pDC | MHC II | IL-23 | Antigen presentation to Th1/Th2/TH17 | (92, 93, 95) | Tolerogenic DC | MHC IIlow | IDO | Antigen presentation to Treg | (98–101) |
cDC | CD80/CD86 | Secretion of inflammatory cytokines | CD80/CD86low | IL-10 | Inhibition of TCR signaling | |||||
moDC | CD1c/CD11b (mice) | PDL-1,-2 | TGF-β | |||||||
CD141/CD103 (mice) | CTLA-4 | galectin-1 | ||||||||
pentraxin 3 | ||||||||||
T-lymphocytes | CD4+ T-helper | CD3 | IFN-γ (in CD4+ Th) | Autoreactivity | (104, 105, 109, 111, 112) | Tregs | CTLA-4 | TGF-β | Secretion of anti-inflammatory cytokines | (102, 104, 110, 114, 115, 118) |
CD8+ T-cytotoxic | CD4 | IL-17 (in CD4+ Th and γδ T cells) | Secretion of inflammatory cytokines | AT2R+ T cells | PD-1 | IL-10 | Apoptosis of inflammatory cells | |||
γδ T cells | CD8 | perforins (in CD8+ Tc) | Cytotoxicity in cardiomyocytes? | BTLA | IL-35 | Increase of extracellular adenosine | ||||
γδ TCR | granzymes (in CD8+ Tc) | CD39 | ||||||||
CD73 | ||||||||||
Myeloid-derived suppressor cells | ? | ? | ? | ? | ? | PMN-MDSC | HLADR-CD14-CD15+CD11b+ | IL-10 | Immune suppression? | (124, 126–128) |
M-MDSC | CD33+CD14+CD11b+ | NO | ||||||||
eMDSC | Lin-CD33+CD11b+ | TGF-β | ||||||||
IDO | ||||||||||
arginase 1 | ||||||||||
B-lymphocytes | B1-lymphocytes | CD19 | IgM | Antibody production | (134, 136) | regulatory B-lymphocytes | Tim-1 | IL-10 | Secretion of anti-inflammatory cytokines? | (138) |
B2-lymphocytes | IgG | Chemokines production | TGF-β? | |||||||
CCL7 | IL-35? | |||||||||
NK-cells | ? | CD69 | IFN-γ | Secretion of inflammatory cytokines | (139–141) | ? | Inhibitory receptors: | IL-13 | Secretion of anti-inflammatory cytokines | (139, 143, 144) |
Activating receptors: | TNF-α | Recognition of DAMPs | KIR | IL-10 | Recognition of “self”-molecules | |||||
NKp44 | perforin | Cytolysis | NKG-2A | Prevention of cytolysis | ||||||
NKG2D | granzyme | |||||||||
CD226 | ||||||||||
iNKT | ? | Activating receptors | IL-17 | Secretion of inflammatory cytokines | (145) | ? | Inhibitory receptors | IL-4 | Secretion of anti-inflammatory cytokines | (147) |
Invariant αβ-TCR | IFN-γ | Recognition of DAMPs | IL-10 | Recognition of “self”-molecules | ||||||
Cytolysis | Prevention of cytolysis |
BTLA, B- and T-lymphocyte attenuator; CCL, CC chemokine ligand; CCR, C-C chemokine receptor; CD, cluster of differentiation; CTLA, cytotoxic T-lymphocyte-associated protein; DAMP, damage associated molecular pattern; DC, dendritic cells; IDO, indoleamine 2,3-dioxygenase; IFN, interferon; Ig, immunoglobulin; IL, interleukin; KIR, killer cell immunoglobulin-like receptor; Lin, lineage; MC, mast cell; MHC, major histocompatibility complex; MMP, matrix metalloproteinase; MPO, myeloperoxidase; NKG2D, natural killer group 2 member D; NO, nitric oxide; PDL, programmed death ligand; ROS, reactive oxygen species; SPM, specialized pro-resolving mediators; TCR, T-cell receptor; TGF, transforming growth factor; TNF, tumor necrosis factor; VEGF, vascular endothelial growth factor. Question marks indicate absent or incomplete data and facts that have not been sufficiently studied for myocardial infarction.