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-gamma 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.
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