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Nat Med. 2002 Apr;8(4):373-8.

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

Author information

1
Molecular Biomedicine, Department of Environmental Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. manfred.kopf@biomed.umnw.ethz.ch

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-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.

PMID:
11927943
DOI:
10.1038/nm0402-373
[Indexed for MEDLINE]

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