Complement component C3 promotes T-cell priming and lung migration to control acute influenza virus infection

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Abstract
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.