Article: article from journal or magazin.
Viral infections induce abundant numbers of senescent CD8 T cells.
Journal of Immunology
Viral infections are often accompanied by extensive proliferation of reactive CD8 T cells. After a defined number of divisions, normal somatic cells enter a nonreplicative stage termed senescence. In the present study we have identified the inhibitory killer cell lectin-like receptor G1 (KLRG1) as a unique marker for replicative senescence of murine CD8 T cells. KLRG1 expression was induced in a substantial portion (30-60%) of CD8 T cells in C57BL/6 mice infected with lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus, or vaccinia virus. Similarly, KLRG1 was found on a large fraction of LCMV gp33 peptide-specific TCR-transgenic (tg) effector and memory cells activated in vivo using an adoptive transfer model. Transfer experiments with CFSE-labeled TCR-tg cells into LCMV-infected hosts further indicated that induction of KLRG1 expression required an extensive number of cell divisions. Most importantly, KLRG1(+) TCR-tg effector/memory cells could efficiently lyse target cells and secrete cytokines, but were severely impaired in their ability to proliferate after Ag stimulation. Thus, this study demonstrates that senescent CD8 T cells are induced in abundant numbers during viral infections in vivo.
Aging/immunology, Animals, CD8-Positive T-Lymphocytes/physiology, Cell Aging, Cell Division, Lectins, C-Type, Lymphocytic Choriomeningitis/immunology, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Inbred DBA, Receptors, Immunologic/analysis, Vaccinia virus, Vesicular stomatitis Indiana virus, Virus Diseases/immunology
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