| First Author | Kohlmeier JE | Year | 2010 |
| Journal | Immunity | Volume | 33 |
| Issue | 1 | Pages | 96-105 |
| PubMed ID | 20637658 | Mgi Jnum | J:162550 |
| Mgi Id | MGI:4819301 | Doi | 10.1016/j.immuni.2010.06.016 |
| Citation | Kohlmeier JE, et al. (2010) Type I interferons regulate cytolytic activity of memory CD8(+) T cells in the lung airways during respiratory virus challenge. Immunity 33(1):96-105 |
| abstractText | Memory CD8(+) T cells in the lung airways provide protection from secondary respiratory virus challenge by limiting early viral replication. Here, we demonstrate that although airway-resident memory CD8(+) T cells were poorly cytolytic, memory CD8(+) T cells recruited to the airways early during a recall response showed markedly enhanced cytolytic ability. This enhanced lytic activity did not require cognate antigen stimulation, but rather was dependent on STAT1 transcription factor signaling through the interferon-alpha receptor (Ifnar1), resulting in the antigen-independent expression of granzyme B protein in both murine and human virus-specific T cells. Signaling through Ifnar1 was required for the enhanced lytic activity and control of early viral replication by memory CD8(+) T cells in the lung airways. These findings demonstrate that innate inflammatory signals act directly on memory T cells, enabling them to rapidly destroy infected host cells once they enter infected tissues. |
