| First Author | Rapaport AS | Year | 2015 |
| Journal | Immunity | Volume | 43 |
| Issue | 6 | Pages | 1112-24 |
| PubMed ID | 26680205 | Mgi Jnum | J:234674 |
| Mgi Id | MGI:5790556 | Doi | 10.1016/j.immuni.2015.11.005 |
| Citation | Rapaport AS, et al. (2015) The Inhibitory Receptor NKG2A Sustains Virus-Specific CD8(+) T Cells in Response to a Lethal Poxvirus Infection. Immunity 43(6):1112-24 |
| abstractText | CD8(+) T cells and NK cells protect from viral infections by killing virally infected cells and secreting interferon-gamma. Several inhibitory receptors limit the magnitude and duration of these anti-viral responses. NKG2A, which is encoded by Klrc1, is a lectin-like inhibitory receptor that is expressed as a heterodimer with CD94 on NK cells and activated CD8(+) T cells. Previous studies on the impact of CD94/NKG2A heterodimers on anti-viral responses have yielded contrasting results and the in vivo function of NKG2A remains unclear. Here, we generated Klrc1(-/-) mice and found that NKG2A is selectively required for resistance to ectromelia virus (ECTV). NKG2A functions intrinsically within ECTV-specific CD8(+) T cells to limit excessive activation, prevent apoptosis, and preserve the specific CD8(+) T cell response. Thus, although inhibitory receptors often cause T cell exhaustion and viral spreading during chronic viral infections, NKG2A optimizes CD8(+) T cell responses during an acute poxvirus infection. |
