[Asp371]-Tyrosinase (369-377) is a naturally occurring tyrosinase antigen peptide.[1] It is formed via post-translational modification of Asn371.[2] [Asp371]-Tyrosinase (369-377) binds to MHC class I subtype HLA-A*0201-positive T2 cells (IC50 = 1.2 µg/ml) and induces lysis of HLA-A2.1-positive T2 cells incubated with cytotoxic T lymphocytes in a concentration-dependent manner.3,1 Immunization with [Asp371]-tyrosinase (369-377)-pulsed, CD40L-activated autologous dendritic cells delays tumor growth in an AAD-expressing B16-F1 melanoma model using transgenic mice expressing HLA-A*0201 linked to the CD8-binding domain of H-2Dd (AAD).[4]
References:
[1].Skipper, J.C.H., R.C., Gulden, P.H., Brichard, V., et al.An HLA-A2-restricted tyrosinase antigen on melanoma cells results from posttranslational modification and suggests a novel pathway for processing of membrane proteinsJ. Exp. Med.83(2)527-534(1996).
[2].Mosse, C.A., Meadows, L., Luckey, C.J., et al.The class I antigen-processing pathway for the membrane protein tyrosinase involves translation in the endoplasmic reticulum and processing in the cytosolJ. Exp. Med.87(1)37-48(1998).
[3].van Elsas, A., van der Burg, S.H., van der Minne, C.E., et al.Peptide-pulsed dendritic cells induce tumoricidal cytotoxic T lymphocytes from healthy donors against stably HLA-A*0201-binding peptides from the Melan-A/MART-1 self antigenEur. J. Immunol.26(8)1683-1689(1996).
[4].Mullis, D.W., Bullock, T.N.J., Colella, T.A., et al.Immune responses to the HLA-A*0201-restricted epitopes of tyrosinase and glycoprotein 100 enable control of melanoma outgrowth in HLA-A*0201-transgenic miceJ. Immunol.67(9)4853-4860(2001).