| First Author | Jeon S | Year | 2013 |
| Journal | J Immunol | Volume | 190 |
| Issue | 12 | Pages | 6277-86 |
| PubMed ID | 23656736 | Mgi Jnum | J:204865 |
| Mgi Id | MGI:5543570 | Doi | 10.4049/jimmunol.1300582 |
| Citation | Jeon S, et al. (2013) PD-L1/B7-H1 regulates the survival but not the function of CD8+ T cells in herpes simplex virus type 1 latently infected trigeminal ganglia. J Immunol 190(12):6277-86 |
| abstractText | HSV type 1 (HSV-1)-specific CD8(+) T cells provide immunosurveillance of trigeminal ganglion (TG) neurons that harbor latent HSV-1. In C57BL/6 mice, the TG-resident CD8(+) T cells are HSV specific and maintain a 1:1 ratio of cells recognizing an immunodominant epitope on viral glycoprotein B (gB498-505-Tet(+)) and cells reactive to subdominant epitopes (gB-Tet(-)). The gB-Tet(-) CD8(+) T cells maintain their frequency in TG by balancing a higher rate of proliferation with a correspondingly higher rate of apoptosis. The increased apoptosis is associated with higher expression of programmed death-1 (PD-1) on gB-Tet(-) CD8(+) T cells and the interaction with PD-1 ligand (PD-L1/B7-H1). IFN-gamma regulated expression of the PD-1 ligand (PD-L1/B7-H1) on neurons bearing higher copies of latent viral genome. In latently infected TG of B7-H1(-/-) mice, the number and frequency of PD-1(+) gB-Tet(-) CD8(+) T cells increases dramatically, but gB-Tet(-) CD8(+) T cells remain largely nonfunctional and do not provide increased protection from HSV-1 reactivation in ex vivo cultures of latently infected TG. Unlike observations in some chronic infection models, B7-H1 blockade did not increase the function of exhausted gB-Tet(-) CD8 T cells in latently infected TG. |
