NOX2 is an enzymatic complex that produce oxygen radicals and is important for killing pathogens. A lack of function mutation in genes coding for NOX2 or its subunits cause a hereditary disease called chronic granulomatous disease (CGD). In addition to recurrent infection, CGD patients are also more prone to develop autoimmunity. This suggests an important role of NOX2 in controlling the adaptive immune response. The aim of this thesis was to study this role. We therefore used ovalbumin (OVA) as antigen and curdlan or alum as adjuvant to study the humoral and T cell response in NOX2-deficient and WT mice. We found that NOX2-deficient mice produced more OVA-specific IgG2c antibodies. This increased antibody production was associated with an enhanced Th1 response. We also demonstrated that NOX2-deficient dendritic cells are more efficient in activating T cells than WT DCs. Finally, NOX2-deficient DCs produce more Th1-driving cytokine that WT DCs.