Lunardi-Iskandar Y, Gessain A, Lam V H, Gallo R C
Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
J Exp Med. 1993 Mar 1;177(3):741-50. doi: 10.1084/jem.177.3.741.
T cell colonies were generated from the peripheral blood mononuclear cells (PBMC) of 10 patients with tropical spastic paraparesis/human T lymphocyte virus type I (HTLV-I)-associated myeloencephalopathy (TSP/HAM), two healthy HTLV-I carriers, and 17 healthy HTLV-I-seronegative subjects. PBMC were cultured in methylcellulose in the absence of added growth factors (spontaneous T cell colonies), or in the presence of phorbol myristate acetate and interleukin 2 (induced T cell colonies). PBMC T cell colony-forming cells (T-CFC) from all TSP/HAM patients and HTLV-I carriers were able to grow in the absence of added growth factors and/or mitogenic stimulation. Pooled spontaneous and induced colonies were composed of cells bearing CD3+, CD4+, CD8+, and CD1+ antigens. Colonies from normal HTLV-I-seronegative subjects displayed mature cells bearing the CD3+, CD4+, CD8+, and CD1- surface phenotype. In addition, spontaneous and induced T cell colonies expressed HTLV-I antigens in 18-38% of the cells from TSP/HAM patients and HTLV-I carriers. These results demonstrate that HTLV-I infection is associated with an abnormal proliferation and differentiation of T cell progenitors in vitro and that the T-CFC from HTLV-I-seropositive individuals are infected, suggesting that T-CFC abnormalities may play a predominant role in the pathophysiology of HTLV-I.
从10例热带痉挛性截瘫/人类T淋巴细胞病毒I型(HTLV-I)相关脊髓病(TSP/HAM)患者、2例健康的HTLV-I携带者以及17例健康的HTLV-I血清学阴性受试者的外周血单个核细胞(PBMC)中生成T细胞集落。PBMC在无添加生长因子的甲基纤维素中培养(自发T细胞集落),或在佛波酯肉豆蔻酸酯和白细胞介素2存在的情况下培养(诱导T细胞集落)。所有TSP/HAM患者和HTLV-I携带者的PBMC T细胞集落形成细胞(T-CFC)在无添加生长因子和/或有丝分裂原刺激的情况下能够生长。合并的自发和诱导集落由携带CD3+、CD4+、CD8+和CD1+抗原的细胞组成。来自正常HTLV-I血清学阴性受试者的集落显示出携带CD3+、CD4+、CD8+和CD1-表面表型的成熟细胞。此外,来自TSP/HAM患者和HTLV-I携带者的细胞中,18%至38%的自发和诱导T细胞集落表达HTLV-I抗原。这些结果表明,HTLV-I感染与体外T细胞祖细胞的异常增殖和分化有关,并且来自HTLV-I血清学阳性个体的T-CFC被感染,提示T-CFC异常可能在HTLV-I的病理生理学中起主要作用。