4.6 Article

The α1β1 integrin and TNF receptor II protect airway CD8+ effector T cells from apoptosis during influenza infection

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JOURNAL OF IMMUNOLOGY
卷 179, 期 8, 页码 5054-5063

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AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.179.8.5054

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  1. NIAID NIH HHS [AI050020] Funding Source: Medline
  2. NIA NIH HHS [AG021970] Funding Source: Medline

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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 a-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-a 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-a 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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