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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.

Original publication

DOI

10.1038/nm0402-373

Type

Journal article

Journal

Nat Med

Publication Date

04/2002

Volume

8

Pages

373 - 378

Keywords

Animals, Antibodies, Viral, Cell Movement, Complement C3, Immunoglobulin G, Interferon-gamma, Lung, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Knockout, Orthomyxoviridae, Orthomyxoviridae Infections, Receptors, Complement 3b, Receptors, Complement 3d, T-Lymphocytes, T-Lymphocytes, Cytotoxic, T-Lymphocytes, Helper-Inducer