Thimme Robert, Appay Victor, Koschella Marie, Panther Elisabeth, Roth Evelyn, Hislop Andrew D, Rickinson Alan B, Rowland-Jones Sarah L, Blum Hubert E, Pircher Hanspeter
Institute for Medical Microbiology and Hygiene, Department of Immunology, Hermann-Herder-Str. 11, University of Freiburg, D-79104 Freiburg, Germany.
J Virol. 2005 Sep;79(18):12112-6. doi: 10.1128/JVI.79.18.12112-12116.2005.
The killer cell lectin-like receptor G1 (KLRG1) is a natural killer cell receptor expressed by T cells that exhibit impaired proliferative capacity. Here, we determined the KLRG1 expression by virus-specific T cells. We found that repetitive and persistent antigen stimulation leads to an increase in KLRG1 expression of virus-specific CD8+ T cells in mice and that virus-specific CD8+ T cells are mostly KLRG1+ in chronic human viral infections (human immunodeficiency virus, cytomegalovirus, and Epstein-Barr virus) but not in resolved infection (influenza virus). Thus, by using KLRG1 as a T-cell marker, our results suggest that the differentiation status and function of virus-specific CD8+ T cells are directly influenced by persistent antigen stimulation.
杀伤细胞凝集素样受体G1（KLRG1）是一种由增殖能力受损的T细胞表达的自然杀伤细胞受体。在此，我们测定了病毒特异性T细胞的KLRG1表达情况。我们发现，重复性和持续性抗原刺激会导致小鼠体内病毒特异性CD8+ T细胞的KLRG1表达增加，并且在慢性人类病毒感染（人类免疫缺陷病毒、巨细胞病毒和爱泼斯坦-巴尔病毒）中，病毒特异性CD8+ T细胞大多为KLRG1阳性，但在已治愈的感染（流感病毒）中并非如此。因此，通过将KLRG1用作T细胞标志物，我们的结果表明，持续性抗原刺激直接影响病毒特异性CD8+ T细胞的分化状态和功能。
