Table 1.

Important activators of NF-κB.

Activator class	Examples
Cytokines	Il-1β, TNFα (25, 26), IL-12 (27), IL-17 (28), IL-33 (29), Lymphotoxin-β (30), GM-CSF (31)
Receptor ligands	CD40L (32), BAFF [B-cell activating factor (33)], CD4-ligand [HIV-gp120, (34)], TRAIL (35), FasL (36), BMP-2 and−4 (37), EGF (38), HGF (39), insulin (40)
Bacteria	Lipopolysaccharide [LPS (41, 42)], flagellin (43), CpG-DNA (44), enterotoxins (45, 46),
Viruses	dsRNA via PKR (47), many viral proteins [as reviewed in: (48)]
Eukaryotic parasites	Candida albicans (49), Entamoeba histolytica (50), Leishmania (51)
Cell lysis products	DAMPs [Danger associated molecular patterns, (52)], HMGB1 (53), extracellular DNA(54), extracellular RNA (55, 56)
Physiological stress	ER stress (57–59), turbulent flow (shear stress) (60–62), acidic pH (63), oxidative stress (64, 65), hyperglycemia (66)
Physical stress	Ionizing radiation (67, 68), UV-light (69, 70), cold (71)
Modified proteins	Advanced glycation end products (AGEs), oxidized LDL, amyloid protein fragments

Viruses not only activate NF-κB—but also often make use of the NF-κB pathway to control their own replication or to prevent apoptosis of host cells; furthermore, some viral genes have NF-κB binding sites and are induced by NF-κB (48).