CD8+ T cells that express CD4 on their surface (CD4dimCD8bright T cells) recognize an antigen-specific target, are detected in vivo, and can be productively infected by T-tropic HIV
CD8+ T cells that express CD4 on their surface (CD4dimCD8bright T cells) recognize an antigen-specific target, are detected in vivo, and can be productively infected by T-tropic HIV
复制标题
DOI：
10.1182/blood-2002-07-1972
复制
发表时间：
2003-09-15
期刊：
影响因子：
20.3
通讯作者：
Al-Harthi, L
中科院分区：
文献类型：
--
作者：
Zloza, A;Sullivan, YB;Al-Harthi, L
CD8(+)T细胞上的CD4可被上调，产生一种CD8(明亮)表型。我们先前证明，CD8(+)T细胞的活化表型是由CD4(Dim)CD8(Light)表型组成的。我们在这里证明，与CD8(+)、CD4(-)和CD4(+)T细胞相比，激活的CD4(Dim)CD8(Bright)T细胞没有发生凋亡，也不产生显著的细胞内干扰素-γ(IFNGamma)、白介素2(IL-2)或白介素10(IL-10)，但细胞内IL-4水平升高。在巨细胞病毒(CMV)多肽(Pp65)的刺激下，CD4(Dim)CD8(Bright)细胞识别CMV pp65四聚体的能力比CD4(-)CD8(+)T细胞高约19倍，这表明这些细胞对抗原的特异性识别能力远远高于CD4(-)CD8(+)T细胞。CD4(Dim)CD8(Bright)T细胞也表达CXCR4和CCR5，但对T嗜性而非M嗜性HIV感染敏感。一种被认为是β-趋化因子的可溶性因子负责抑制CD4(Dim)CD8(Bright)T细胞中M嗜M的HIV感染。HIV+患者的CD8(+)T细胞能够上调CD8(+)T细胞表面的CD4。我们还提供了HIV+患者外周血中存在CD4(Dim)CD8(Bright)T细胞的证据，尽管频率很低。总而言之，这些数据表明，CD4(Dim)CD8(Bright)T细胞在正常T细胞生物学和HIV发病机制中都发挥了作用。(C)2003年，由美国血液病学会提供。
CD4 can be up-regulated on CD8(+) T cells generating a CD4(dim)CD8(bright) phenotype. We previously demonstrated that the CD4(dim)CD8(bright) phenotype constitutes an activated phenotype of CD8(+) T cells. We demonstrate here that the activated CD4(dim)CD8(bright) T cells are not undergoing apoptosis and do not produce significant intracellular levels of interferon gamma (IFNgamma), interleukin 2 (IL-2), or IL-10 but express elevated levels of intracellular IL-4 in comparison to CD8(+)CD4(-) and CD4(+) T cells. In response to cytomegalo-virus (CMV) peptide (pp65) priming, CD4(dim)CD8(bright) cells recognized CMV pp65 tetramer approximately 19-fold higher than CD4(-)CD8(+) T cells, indicating that these cells are capable of antigen-pecific recognition to a far greater extent than CD4(-)CD8(+) T cells. CD4(dim)CD8(bright) T cells also express both CXCR4 and CCR5 but are susceptible to T-tropic and not M-tropic HIV infection. A soluble factor believed to be beta-chemokine is responsible for the inhibition of M-tropic HIV infection in CD4(dim)CD8(bright) T cells. CD8(+) T cells from HIV+ patients were capable of up-regulating CD4 on CD8(+) T cells. We also provide evidence of the presence of peripheral blood CD4(dim)CD8(bright) T cells in HIV+ patients, albeit at low frequency. Collectively, these data suggest a role of CD4(dim)CD8(bright) T cells in both normal T-cell biology and HIV pathogenesis. (C) 2003 by The American Society of Hematology.