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Different Immunologic Microenvironments in Halo Nevi and Melanomas

In halo nevi, the nevus cells get destroyed with the passage of time. A complete regression is rare even with brisk lymphocytic infiltrate in melanomas. We compared the immunologic microenvironments in these entities in order to understand better the regression mechanism in these lesions. We found that the ratio of CD8+/CD4+ cells was comparable in nevi and melanomas, Foxp3+/CD4+ was 1/2 and 1/15, respectively, which was much higher in halo nevi. Perforin+ T cells counted 60% of the CD8+ cells in halo nevi, while they were less than 5% in melanomas. We concluded that the majority of tumor‐infiltrating CD8+ T cells express perforin, suggesting that perforin‐mediated cytotoxicity may be the key mechanism involving the early regression of halo nevi. Increased Foxp3+ Treg most likely reflect the negative feedback mechanisms to prevent tissue damage from severe immunoreaction in halo nevi. Although CD8+ T cells significantly increase in melanomas similarly to in halo nevi, these T cells lack perforin, suggesting defective CTL around tumor, which may contribute to the mechanisms of immune evasion leading to the aggressive growth of the tumor. The failed immunoreaction in melanomas does not cause tissue damage, which may reflect to the paucity of Foxp3+ T cells in melanomas. In an attempt to study what mechanisms inactivate effector CTL independent of Treg, we found many TGF‐β‐secreting cells in melanomas but none in halo nevi. Indeed, melanoma regressed upon combination treatment of TGF‐β blockade and anti‐41BB in a murine model. Our study suggested that immune suppressive cytokines in the tumor environment may be important factors independent of Treg to suppress anti‐tumor immunity.