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. 2020 Jun 1;17:19. doi: 10.1186/s12989-020-00349-z

Table 3.

In vitro studies on immunological properties of NPs

NPs cell response cell frequence/activity Potential effect
TiO2 (6-48 h) ↗ oxidative stress (ROS) [121–125] ↗ DC, μɸ, lymphocytes [121, 122, 126] Innate inflammatory response [122, 126–128]
↗ expression of TLR (TLR3, TLR4, TLR7 and TLR10) [126, 128] ↗ naïve T cells [122] Cytotoxicity and inflammation [122, 123, 125, 129]
↗ pro-inflammatory cytokines (IL-6, TNF-α, IL1-β) [121–123, 127, 130–132] ↗ mature DC [122, 131, 132] Adjuvant [121, 130–132]
↗ chemokines secretion (IL-8 and CXCL1) ↙ activity (IL-8) [122, 133] ↗ mast cell activation [134] Allergic response [134, 135]
↗ co-stimulatory molecules (CD80 and CD86) [122, 123, 131, 132] ↙ neutrophil and μɸ mobility [133] Tissue damage [124, 133]
↗ MPO, MMP-9 and NET [124, 136] ↗ neutrophil activity [124, 136] NETosis: inflammation, necrosis and apoptosis [124]
↗ β-hexosaminidase release [134]
inflammasome activation [123]
activation of NFkB pathway [128, 131]
SiO2 (6-48 h) ↗ apoptose [123, 125, 137, 138] ↙ DC and lymphocytes [123, 137, 138] Imbalance of immune response [125, 126, 137–140]
↗ pro inflammatory cytokines (IL1-β, IL-2, TNF-α) [121, 123, 126, 138, 139, 141] ↗ DC maturation [123, 139] Immunogenic or adjuvant potential [121, 123, 126, 140, 141]
↗ CD80, CD86 and MHCII [123, 138, 139] ↗ M1 μɸ polarization [126, 140] Inflammation [121, 123, 125, 126, 137–141]
↙ TLR9 expression [126] ↗ neutrophil activity [142] ↗ Susceptibility IBD [123, 126, 140], autoimmune diseases [139, 140]
↗ oxidative stress (ROS) [125] ↗ cross-presentation [141] NETosis: inflammation, necrosis and apoptosis [142]
inflammasome activation [123] Cytotoxic effect [121, 123, 125, 137, 138, 140]
NFkB activation [138] Susceptibility to infection [126]
↗ DNA release – NET [142] Allergic response [135]
ZnO (6-48 h) ↗ pro inflammatory cytokines (IL-1β, TNF-α, IL-6, IFN-ɣ) [125, 130, 143, 144] ↗ DC activity [130, 145] Cytotoxicity and inflammation [125, 129, 130, 134, 143, 146]
↗ chemokines secretion (IL-8, CXCL9) [130, 144] ↙ Lymphocytes [146] Imbalance of immune response [125, 129, 130, 143, 144]
↗ oxidative stress (ROS) [125, 145] ↗ neutrophil functions [136] Chronic pathologies [143]
induces neo-synthesis of polypeptides [144] ↙ mast cell activation [134] Allergenic response [134, 135]
↙ or ↗ apoptose [125, 129, 130, 144] ↗ eosinophils [144] Protective effect [134, 144]
↗ DNA damage [125, 129, 146] Genomic instability [146]
↙ β-hexosaminidase and histamine release [134] Cell cycle imbalanced [125]
Ag (6-48 h) ↗ oxidative stress (ROS) [147–149] ↙ μɸ, lymphocyte [147–149] Apoptosis and cytotoxicity [147–149]
↗ DNA damage [148] ↗ mast cell activation [135, 150, 151] Inflammation/imbalance of immune response [147–149]
↗ pro inflammatory cytokines (IL-1β, TNF-α) [147, 149] Allergic response [135, 150, 151]
inflammasome activation [147]
↗ β-hexosaminidase release [135, 150, 151]

CD Cluster of differentiation, CXCL1 chemokine ligand 1, DC dendritic cell, IBD Inflammatory bowel disease, Ig immunoglobulin, IL interleukin, μɸ macrophage, MHCII major histocompatibility complex II, MMP-9 matrix metalloproteinase 9, MPO myeloperoxidase, NET Neutrophil extracellular trap, NFkB nuclear factor-kappa B, ROS reactive oxygen species, TLR Toll-like receptor