[HTML][HTML] CD8+ T cells with an intraepithelial phenotype upregulate cytotoxic function upon influenza infection in human lung

B Piet, GJ de Bree, BS Smids-Dierdorp… - The Journal of …, 2011 - Am Soc Clin Investig
B Piet, GJ de Bree, BS Smids-Dierdorp, CM van der Loos, EBM Remmerswaal
The Journal of clinical investigation, 2011Am Soc Clin Investig
The human lung T cell compartment contains many CD8+ T cells specific for respiratory
viruses, suggesting that the lung is protected from recurring respiratory infections by a
resident T cell pool. The entry site for respiratory viruses is the epithelium, in which a subset
of lung CD8+ T cells expressing CD103 (αE integrin) resides. Here, we determined the
specificity and function of CD103+ CD8+ T cells in protecting human lung against viral
infection. Mononuclear cells were isolated from human blood and lung resection samples …
The human lung T cell compartment contains many CD8+ T cells specific for respiratory viruses, suggesting that the lung is protected from recurring respiratory infections by a resident T cell pool. The entry site for respiratory viruses is the epithelium, in which a subset of lung CD8+ T cells expressing CD103 (αE integrin) resides. Here, we determined the specificity and function of CD103+CD8+ T cells in protecting human lung against viral infection. Mononuclear cells were isolated from human blood and lung resection samples. Variable numbers of CD103+CD8+ T cells were retrieved from the lung tissue. Interestingly, expression of CD103 was seen only in lung CD8+ T cells specific for influenza but not in those specific for EBV or CMV. CD103+ and influenza-reactive cells preferentially expressed NKG2A, an inhibitor of CD8+ T cell cytotoxic function. In contrast to CD103CD8+ T cells, most CD103+CD8+ cells did not contain perforin or granzyme B. However, they could quickly upregulate these cytotoxic mediators when exposed to a type I IFN milieu or via contact with their specific antigen. This mechanism may provide a rapid and efficient response to influenza infection, without inducing cytotoxic damage to the delicate epithelial barrier.
The Journal of Clinical Investigation