Vanasek Tracy L, Nandiwada Sarada L, Jenkins Marc K, Mueller Daniel L
Department of Medicine, Center for Immunology, University of Minnesota Medical School, 312 Church Street SE, Minneapolis, MN 55455, USA.
J Immunol. 2006 May 15;176(10):5880-9. doi: 10.4049/jimmunol.176.10.5880.
T cell clonal anergy induction in lymphopenic nu/nu mice was found to be ineffective. Exposure to a tolerizing peptide Ag regimen instead induced aggressive CD4(+) cell cycle progression and increased Ag responsiveness (priming). Reconstitution of T cell-deficient mice by an adoptive transfer of mature peripheral lymphocytes was accompanied by the development of a CD25(+)Foxp3(+)CTLA-4(+)CD4(+) regulatory T cell population that acted to dampen Ag-driven cell cycle progression and facilitate the induction of clonal anergy in nearby responder CD25(-)CD4(+) T cells. Thus, an early recovery of CD25(+) regulatory T cells following a lymphopenic event can prevent exuberant Ag-stimulated CD4(+) cell cycle progression and promote the development of clonal anergy.
研究发现，在淋巴细胞减少的裸鼠中诱导T细胞克隆无能是无效的。相反，暴露于耐受性肽抗原方案会诱导CD4(+)细胞周期的快速进展并增强抗原反应性（致敏）。通过过继转移成熟外周淋巴细胞来重建T细胞缺陷小鼠，会伴随着CD25(+)Foxp3(+)CTLA-4(+)CD4(+)调节性T细胞群体的出现，该群体可抑制抗原驱动的细胞周期进展，并促进附近应答性CD25(-)CD4(+)T细胞中克隆无能的诱导。因此，淋巴细胞减少事件后CD25(+)调节性T细胞的早期恢复可防止抗原刺激引起的CD4(+)细胞周期过度进展，并促进克隆无能的发展。
