Nous avons inhibé l expression de l insulin-like growth factor I sur une lignée de cellules de mélanome (la lignée B16-F0 des souris C57Bl/6). Les molécules impliquées dans l immunité (CMH-I, B7.1) n ont montré aucune variation d expression suite à la modulation de IGF-I. Par contre, la molécule de tétraspanine CD9, impliquée dans les interactions cellulaires, s est trouvée fortement inhibée. En parallèle, l inoculation in vivo de la lignée modifiée (B16-F0.MOD) induit une diminution de la tumorigénicité et améliore la survie. La vaccination par B16-F0.MOD entraîne la formation d effecteurs humoraux lytiques en présence de complément dirigés contre la lignée parentale, mais également d effecteurs cellulaires. En particulier, la sous-population CD8+ a la capacité d inhiber la croissance tumorale in vivo et la prolifération cellulaire in vitro. En conclusion, l inhibition de l IGF-I a provoqué la production d effecteurs immuns anti-mélanomeWe developed a strategy of immunological treatment based on inhibition of the insulin-like growth factor I (IGF-I) in melanoma cell line (B16-F0 from C57Bl/6 mice). Immunological molecules (CMH-I, B7.1) weren t modulated by targeting IGF-I. On the other hand, downregulation of the tetraspanin molecule named CD9, implicated in cellular interactions, was observed. Moreover, delayed outgrowth and increased survival were evaluated after inoculation of modified cells in syngeneic hosts. Vaccines were realised using these blocked modified cells. Cytotoxic antibodies were shown to be present in the sera of mice that were able to lyse parental cells in the presence of rabbit complement. Moreover, spleen cells from CD8 subpopulation harvested from hosts vaccinated were able to inhibit in vivo outgrowth and in vitro proliferation of parental B16-F0. Consequently promising results were reported using IGF-I inhibition strategy leading to stimulate anti-melanoma immune effectorsPARIS-BIUP (751062107) / SudocSudocFranceF