. Author manuscript; available in PMC: 2010 Nov 1.

Published in final edited form as: J Autoimmun. 2009 Oct 12;33(3-4):239–246. doi: 10.1016/j.jaut.2009.09.004

Table 3.

MHC Class II-binding synthetic peptides used to probe interaction of Tregs and class II expression

MHC Class II restriction	Name	Derivation	Amino acid sequence^a	Thyroiditogenic^b
H2E^b	hTg179	hTg	`NTTDMMIFDLVHSYNRFPD`	Yes
	mTg179	mTg	`NTTDMMIFDLIHNYNRFPD`	Yes
	hTg410	hTg	`QSQQFSVSENLLKEA`	Yes
	mTg409	mTg	`HYQRLSESLLREA`	Yes
	hTg1241	hTg	`GPLICSLESGRWESQ`	No
	hTg2344	hTg	`LTWVQTHIRGFGGDPR`	Yes

H2A^b	mTg1677	mTg	`QNVLSGLYSPVVFSAS`	Yes
	mTg1744	mTg	`WRDTSATQANATCAG`	-
	mTg2051	mTg	`SFCPSAALQSLTEEK`	-
	mTg2086	mTg	`KHFDVAHISTAATSN`	-
	mTg2342	mTg	`LTWVQSHIGAFGGDPQ`	-
	Eα52–68	H2Eα	`ASFEAQGALANIAVDKA`	-

Bolded amino acid indicates predicted MHC class II anchor residue.

Indicates whether peptide is able to expand Tg-primed cells to transfer thyroiditis to naive mice and/or is itself directly thyroiditogenic. Peptide Eα52–68 is not a Tg-derived peptide, and so was not tested for thyroiditogenicity. -; not determined.