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.
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Authors | Manfred Kopf, Brian Abel, Awen Gallimore, Michael Carroll, Martin F Bachmann |
Journal | Nature medicine
(Nat Med)
Vol. 8
Issue 4
Pg. 373-8
(Apr 2002)
ISSN: 1078-8956 [Print] United States |
PMID | 11927943
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antibodies, Viral
- Complement C3
- Immunoglobulin G
- Receptors, Complement 3b
- Receptors, Complement 3d
- Interferon-gamma
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Topics |
- Animals
- Antibodies, Viral
(biosynthesis)
- Cell Movement
(immunology)
- Complement C3
(deficiency, genetics, physiology)
- Immunoglobulin G
(biosynthesis)
- Interferon-gamma
(biosynthesis)
- Lung
(immunology, pathology)
- Lymphocyte Activation
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Orthomyxoviridae
(immunology)
- Orthomyxoviridae Infections
(immunology, pathology)
- Receptors, Complement 3b
(deficiency, genetics, physiology)
- Receptors, Complement 3d
(deficiency, genetics, physiology)
- T-Lymphocytes
(immunology, pathology, physiology)
- T-Lymphocytes, Cytotoxic
(immunology)
- T-Lymphocytes, Helper-Inducer
(immunology)
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