Synthetic peptides derived from the melanocyte-stimulating hormone receptor MC1R can stimulate HLA-A2-restricted cytotoxic T lymphocytes that recognize naturally processed peptides on human melanoma cells
- Flavio Salazar-Onfray,
- Tsutomu Nakazawa,
- Vijay Chhajlani,
- Max Petersson,
- Klas Kärre,
- Giuseppe Masucci
- Karolinska Institutet,
- Uppsala University,
- AstraZeneca,
- Cytel Corporation,
- National Institutes of Health
Sustainable Development Goals
- SDG 3 Good Health and Well
Abstract
Human melanoma-specific HLA-A2 restricted CTLs have recently been shown to recognize antigens expressed by melanoma lines and normal melanocytes, including Melan-A/Mart-1, gp100, gp75, and tyrosinase. Herein, we define HLA- A2-restricted CTL epitopes from a recently cloned melanocortin 1 receptor (MC1R), which belongs to a new subfamily of the G-protein-coupled receptors expressed on melanomas and melanocytes. Thirty-one MC1R-derived peptides were selected on the basis of HLA-A2-specific motifs and tested for their HLA-A2 binding capacity. Of a group of 12 high or intermediate HLA-A2 binding peptides, three nonamers, MC1R244 (TILLGIFFL), MC1R283 (FLALIICNA), and MC1R291 (AIIDPLIYA), were found to induce peptide-specific CTLs from peripheral blood mononuclear cells of healthy HLA-A2+ donors after repeated in vitro stimulation with peptide-pulsed antigen-presenting cells. The CTLs raised against these three HLA-A2+-restricted peptides could recognize naturally processed peptides from HLA-A2+ melanomas and from Cos7 cells cotransfected with MC1R and HLA-A2. CTLs induced by the MC1R291 peptide (but not induced or induced only to a very low extent by the other two MCR1 peptide epitopes) showed cross-reactions with two other members of the melanocortin receptor family, which are more broadly expressed on other tissues. Taken together, our findings have implications in relation both to autoimmunity and immunotherapy of malignant melanomas.
Publication Information
Output type
Original language
English (US)Pages from-to (Number of pages)
Pages 4348-4355 (8 pages)Journal (Volume, Issue Number)
Cancer Research (Volume 57, Issue 19)Publication milestones
- Published - 10/01/1997
Publication status
ISSN
0008-5472Publication IDs
- Scopus: 0030804305
- PubMed: 9331097
