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cells 4 days after tumor implantation. It is of importance to notę that in vivo depletion with anti-NKl.l antibody is complement-mediated, thus reąuired prior to CVF treatment. We found that in the absence of NK cells, CVF treatment had no effect on tumor implantation and early development demonstrating that NK cells were necessary for the decreased tumor growth observed following decomplementation (Fig. 4A).

Considering that T celi activation in the spleen is also increased in the absence of complement, we wanted to determine if decomplementation also affected the induction of tumor-specific cytotoxic T lymphocytes. As assessed by intracellular cytokine staining of gp33 peptide-stimulated T cells from decomplemented and control B16gp33-bearing mice, we found that complement inhibition led to higher levels of tumor-specific (gp33) T cells secreting mainly TNFa (Fig. 4B). Accordingly, the enhancement of gp33-specific CTL induction by CVF was also abolished in the absence NK cells indicating that the effect of decomplementation on early tumor growth is largely mediated by CTLs (Fig. 4B). However, CVF-mediated decomplementation did not lead to superior levels of gp33-specific cytotoxicity as assessed by CD107a expression, a marker of recent degranulation (Fig. 4C). Thus, in the BI6 melanoma model, we demonstrate that CVF treatment limits early tumor growth and promotes a better availability of spienić and tumoral NK cells. This suggests that complement components and NK cells internet thus modulating tumor-specific CTL induction.

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