期刊
JOURNAL OF IMMUNOLOGY
卷 190, 期 12, 页码 6277-6286出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1300582
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资金
- National Eye Institute [P30-EY08098, R01-EY005945, T32-EY017271]
- National Institutes of Health [R56AI85110]
- Research to Prevent Blindness (New York, NY)
- Eye and Ear Foundation of Pittsburgh
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 (gB(498-505)-Tet(+)) and cells reactive to subdominant epitopes (gB-Tet 2). 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.
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