Melanomas are most frequently infiltrated by actively proliferating T-lymphocytes (1 ). Some of these T-cells are cytolytic and recognize peptide antigens derived from melanoma-specific antigens (2 ). However, with the noteworthy exception of rare immune-mediated, sponaneous regressions of melanomas (3 ), or in the particular case of the halo nevus phenomenon in which normal melanocytes are killed by CD8+ -specific T-cells (4 ), the ongoing melanocyte-specific T-cell responses are most frequently incapable of controlling the growth of the tumor, resulting in the malignant melanocytic tumors escaping an otherwise specific immune T-cell response. The understanding of the mechanisms that underlie the switch of efficient to inefficient (and vice versa) T-cell responses is thus of primary importance in conceiving specific immunotherapies of melanomas.
