Abstract |
Primary viral infections of the lung induce potent effector CD8 T cell responses. To function in the influenza-infected airways, CD8 T cells must be able to resist cell death. The majority of the CD8 T cells in the airways and lung parenchyma expressed CD49a, the alpha-chain of the type IV collagen receptor VLA-1, and these cells were highly activated, producing both IFN-gamma and TNF-alpha. In the airways, where type IV collagen is abundant, but not the spleen, the CD49a(+) CD8 cells had reduced proportions of annexin V and caspase 8, and >80% expressed the TNF-alpha receptor II, while Fas, TNFR-I, and CD27 expression were similar to CD49a(-) cells. Furthermore, the CD49a(+), but not CD49a(-), CD8 T cells from the airways were resistant to active induction of apoptosis in the presence of type IV collagen and TNF-alpha in vitro. We propose that TNFR-II and the VLA-1 synergize to protect effector CD8 T cells in the infected airways from apoptosis during the acute infection.
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Authors | Martin V Richter, David J Topham |
Journal | Journal of immunology (Baltimore, Md. : 1950)
(J Immunol)
Vol. 179
Issue 8
Pg. 5054-63
(Oct 15 2007)
ISSN: 0022-1767 [Print] United States |
PMID | 17911590
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Integrin alpha1
- Integrin alpha1beta1
- Receptors, Tumor Necrosis Factor, Type II
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Topics |
- Animals
- Apoptosis
(immunology)
- CD8-Positive T-Lymphocytes
(immunology, metabolism, pathology)
- Cell Separation
- Female
- Immunophenotyping
- Influenza A Virus, H3N2 Subtype
(immunology)
- Integrin alpha1
(biosynthesis, metabolism)
- Integrin alpha1beta1
(physiology)
- Mice
- Mice, Inbred C57BL
- Orthomyxoviridae Infections
(immunology, metabolism, pathology)
- Receptors, Tumor Necrosis Factor, Type II
(physiology)
- Respiratory Mucosa
(immunology, metabolism, pathology)
- T-Lymphocyte Subsets
(immunology, metabolism, pathology)
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