The complement cascade defines an important link between the innate and the specific immune system. Here we show that mice deficient for the third component of complement (C3^−/− mice) are highly susceptible to primary infection with influenza virus. C3^−/− mice showed delayed viral clearance and increased viral titers in lung, whereas mice deficient for complement receptors CR1 and CR2 (Cr2^−/− mice) cleared the infection normally. Priming of T-helper cells and cytotoxic T cells (CTLs) in lung-draining lymph nodes was reduced, and the recruitment into the lung of virus-specific CD4⁺ and CD8⁺ effector T cells producing interferon-γ was severely impaired in C3^−/− but not in Cr2^−/− mice. Consequently, T-helper cell–dependent IgG responses were reduced in C3^−/− mice but remained intact in Cr2^−/− mice. These results demonstrate that complement induces specific immunity by promoting T-cell responses.