Table 1.

Immune responses in neurodegenerative disorders

Disorder	Innate immune response	Adaptive immune response	References
Alzheimer’s disease	TLR2 and TLR4 increased on microglia in AD brains. Aβ induces TLR expression in vitro. Increased pro-inflammatory cytokines and complement components are present around Aβ plaques	T-cell recruitment after Aβ injection. TNF-α and IFN-γ production	8–12,17,22,23,26,34
Parkinson’s disease	TLR2, TLR5 and CD14 increases in PD CNS. Activated NK cells. Microglial activation. Increased expression of CD14 and TLR4 in the substantia nigra of an MPTP animal model	Increases of CD4+ T cells, CD4+ T cells infiltrate in PD brains, influence of Fas ligands, but not of IFN-γ	8–10,23,26
Amyotrophic lateral sclerosis	TLR3 in Purkinje neurons. TLR1,2,7,9 and CD14 expression in ALS	Increase in complement components. Alterations in peripheral levels of CD4+ and CD8+ T cells	8–10,26,35,37
Traumatic brain injury	Myd88 involvement in inflammation following TBI, independently of TLR2/4	CD4 and CD8 infiltration in the acute and chronic phases of TBI	7,38
Stroke	Up-regulation of TLRs on endothelium, neurons and glia	Bias towards Th2 responses	8–10
Paraneoplastic disorders		Antibodies to neuronal antigens	26
Systemic lupus erythematous	IgG autoantibody, complement C4 on necrotic cells	Antibodies to double-stranded DNA	26,27
Multiple sclerosis	NK cells, microglial activation	CD4 and CD8 T cells close to neurons	6,13–15,18–20,26,32,33

Aβ, amyloid-beta; AD, Alzheimer’s disease; ALS, amyotrophic lateral sclerosis; CNS, central nervous system; IFN-γ, interferon-γ; MPTP, 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine; NK, natural killer; PD, Parkinson’s disease; TBI, traumatic brain injury; TNF-α, tumour necrosis factor-α; TLR, toll-like receptor.