Table 1.

Amyloid-β (Aβ) T-cell epitopes and responsiveness in several MHC II and HLA genetic backgrounds

	Strain/MHC II or HLA	Aβ1–42 T-cell responsiveness	T-cell epitope within Aβ residues	References
Mice	C57BL/6 / I-Ab	+	16–30	30–32,113
	SJL / I-As	+++	10–24	30,31
	BALB/c / I-Ad	++	1–28	113
	NOD / I-Ag7	+++	10–24	30
Congenic mice	C57BL/6 / I-As	+	10–24	31
	NOD / I-Ab	+	16–30	30
Humanized mice	DR15	+++	25–42	27
	DR4	+ ++	16–33 1–16, 1–28	27,32
	DRB1*0101	++	1–28	113
	DR3	+	1–16	32
	DQ8	+	1–42	32
Human subjects	DRB1*0101/1301/1001	ND	15–35	27
	DRB1*0401/0404	ND	18–32	27
	DRB1*1501	ND	25–42	27

ND, not determined.

In mice, Aβ-reactive T cells were analysed following Aβ1–42 immunization and re-stimulation with Aβ1–42 or with shorter Aβ peptides in vitro. In human subjects, Aβ T-cell epitopes were analysed in isolated peripheral blood mononuclear cells stimulated initially with Aβ1–42 and thereafter with 15-residue-long overlapping peptides between 1 and 42 residues of Aβ. T-cell responsiveness was measured by the magnitude of antigen-driven T-cell proliferation and cytokine production following immunization. In humanized mice bearing the DRB1 1501 and 0401 alleles, peptides between residues 25 and 42 and between residues 18 and 32 served as the dominant T-cell epitopes, as observed also for T-cell lines derived from human subjects with these HLA genetic backgrounds.²⁶ Aβ42 immunization of humanized HLA-DR4 and HLA-DR3/DQ8 transgenic mice evoked Aβ-reactive T-cell responses which could be partially stimulated by Aβ1–16,³² and DRB1 0101 humanized mice elicited T-cell responses to an epitope between residues 1–28.¹¹³ Since overlapping peptides between residues 15 and 42 of Aβ were not used in these studies, it is unclear whether additional weak T-cell epitopes are located at the N-terminus of Aβ or whether a truncated portion of the epitope was presented to the T cells