Innate Immunity and Neuroinflammation

Table 2

Exogenous and endogenous ligands of toll-like receptors.

Ligand	TLR	Implications/comments	References
Lipopolysaccharide	TLR4	Recognition of Gram (−) bacteria	[117]
Triacylated lipopeptides	TLR1 and TLR2	Recognition of Gram (−) bacteria and mycobacteria	[118]
Diacylated lipopeptides	TLR2 and TLR6	Recognition of Gram (+) bacteria and mycoplasma	[119, 120]
Lipoteichoic acid	TLR2	Recognition of Gram (+) bacteria	[121]
Zymosan	TLR2	Recognition of fungi	[122]
Double-stranded RNA	TLR3	Recognition of virus	[123]
Single-stranded RNA	TLR7 and TLR8	Recognition of virus	[124, 125]
Flagellin	TLR5	Recognition of Gram (−) bacteria	[126]
Unmethylated CpG DNA	TLR9	Recognition of bacteria and virus	[127, 128]
β-amyloid	TLR2; TLR4; TLR4 and TLR6	Neuroinflammation in Alzheimer’s disease	[95, 96, 129, 130]
Mitochondrial DNA	TLR9	Pathogenesis of myocarditis and heart failure	[128]
Lung surfactant protein-A and -D	TLR4; TLR2	Innate immune component of lung. Act as opsonin and macrophage activator. Physiological implications of excessive activation by TLR is not known	[131–133]
Tenascin-C	TLR4	Maintenance and pathogenesis of inflammation in rheumatoid arthritis	[134, 135]
Fibrinogen	TLR4	Present normally in serum and activation has been implicated in rheumatoid arthritis and atherosclerosis	[136, 137]
Oxidised low-density lipoprotein	TLR4	Pathogenesis of atherosclerosis	[95]
MicroRNA let-7	TLR7	Pathogenesis of neurodegeneration	[138]