Martina Maria N, Noel Sanjeev, Saxena Ankit, Rabb Hamid, Hamad Abdel Rahim A
1] Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA [2] Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Immunol Cell Biol. 2015 Mar;93(3):305-10. doi: 10.1038/icb.2014.99. Epub 2014 Nov 25.
CD4(-)CD8(-)double negative (DN) αβ T cells are legitimate components of the normal immune system. However, they are poorly understood and largely ignored by immunologists because of their historical association with the lymphoproliferation that occurs in mice (lpr and gld) and humans (autoimmune lymphoproliferative syndromes patients) with impaired Fas-mediated apoptosis where they are considered abnormal T cells. We believe that the traditional view that DN T cells that cause lymphoproliferation (hereafter referred to as lpr DN T cells) are CD4 and CD8 T cells that lost their coreceptor, conceived more than two decades ago, is flawed and that conflating lpr DN T cells with DN T cells found in normal immune system (hereafter referred to as nDN T cells) is unnecessarily dampening interest of this potentially important cell type. To begin rectifying these misperceptions, we will revisit the traditional view of lpr DN T cells and show that it does not hold true in light of recent immunological advances. In lieu of it, we offer a new model proposing that Fas-mediated apoptosis actively removes normally existing DN T cells from the periphery and that impaired Fas-mediated apoptosis leads to accumulation of these cells rather than de novo generation of DN T cells from activated CD4 or CD8 T cells. By doing so, we hope to provoke a new discussion that may lead to a consensus about the origin of lpr DN T cells and regulation of their homeostasis by the Fas pathway and reignite wider interest in nDN T cells.
CD4(-)CD8(-)双阴性(DN)αβ T细胞是正常免疫系统的合理组成部分。然而,由于它们在历史上与Fas介导的细胞凋亡受损的小鼠(lpr和gld)和人类(自身免疫性淋巴细胞增生综合征患者)中发生的淋巴细胞增生有关,在这些情况下它们被视为异常T细胞,因此免疫学家对它们了解甚少且大多忽略了它们。我们认为,二十多年前所设想的导致淋巴细胞增生的DN T细胞(以下简称lpr DN T细胞)是失去共受体的CD4和CD8 T细胞这一传统观点是有缺陷的,并且将lpr DN T细胞与正常免疫系统中发现的DN T细胞(以下简称nDN T细胞)混为一谈不必要地抑制了对这种潜在重要细胞类型的研究兴趣。为了开始纠正这些误解,我们将重新审视关于lpr DN T细胞的传统观点,并表明鉴于最近的免疫学进展,该观点并不成立。取而代之的是,我们提出了一个新模型,该模型认为Fas介导的细胞凋亡会主动从外周清除正常存在的DN T细胞,而Fas介导的细胞凋亡受损会导致这些细胞的积累,而不是由活化的CD4或CD8 T细胞重新产生DN T细胞。通过这样做,我们希望引发一场新的讨论,这场讨论可能会就lpr DN T细胞的起源以及Fas途径对其稳态的调节达成共识,并重新点燃对nDN T细胞更广泛的研究兴趣。