Role of HTLV-I infection in development of chronic inflammatory arthropathy.

1. 人t淋巴细胞I型病毒感染人滑膜细胞：滑膜细胞的增殖和粒细胞巨噬细胞集落刺激因子的产生。为了确定滑膜细胞是否感染了HTLV-I，以及感染的滑膜细胞是否能够积极增殖并产生细胞因子，我们将滑膜细胞与产生HTLV-I的T细胞系共培养。免疫组化方法表明，第5代滑膜细胞与产生htlv - 1的T细胞共培养后表达htlv - 1抗原。采用聚合酶链反应（PCR）在滑膜细胞中检测HTLV-I前病毒DNA。与htlv - 1感染的T细胞系共培养后，滑膜细胞增殖和转化活性增强。滑膜细胞的增殖对滑膜细胞和htlv - i产生T细胞系的接触至关重要。此外，htlv -i感染的滑膜细胞产生大量的粒细胞巨噬细胞集落刺激因子（GM-CSF）。这些结果表明htlv - 1可能引起慢性炎性关节病，类似于在类风湿性关节炎中发现的情况。HTLV-L pX基因转染U937细胞。采用DEAE葡聚糖法转染U937细胞HTLV-L pX基因。转染HTLV-L pX基因的U937细胞，northern印迹法检测pX MRNA， western印迹法检测Tax蛋白。A-IT-2细胞表达IL-2 Ra mRNA，而转染的U937细胞则不表达。而转染后的U937细胞检测到c-fgr mRNA和p58^<c-fgr>.3。HTLV-I型人嗜t细胞病毒（HTLV-I）包膜合成肽感染个体的不同b细胞应答我们分别以HTLV-I-gag杂交蛋白和HTLV-I-env编码合成肽作为抗原，研究了来自同一HTLV-I流行区HTLV-I感染个体对病毒蛋白的抗体活性差异和抗HTLV-I包膜抗体的特异性差异。htlv -i感染的多发性关节炎患者产生特异性抗体VlE1（残基342-363）和VIE8（残基191-209）。HTLV-I相关性脊髓病（HAM）患者产生VIE7（97-111）和VIE9（268-286）表位的抗体。htlv - 1感染的多发性关节炎患者血清中抗htlv - 1抗体的活性与正常htlv - 1携带者血清中抗htlv - 1抗体的活性无明显差异，且未检测到关节炎患者独有的包膜肽特异性。少

1. Infection of human synovial cells by human T-cell lymphotropic virus Type I : proliferation and granulocyte macrophage-colony stimulating factor production of synovial cells. To determine whether synovial cells are infected with HTLV-I and the infected synovial cells are able to proliferate actively and produce cytokines, the synovial cells were cocultured with HTLV-I-producing T cell lines. The synovial cells in the 5th passage after cocultivation with HTLV-I-producing T cells were shown to express the HTLV-L antigens by an immunohistochemical methods. The HTLV-I proviral DNA was also detected in the synovial cells by the polymerase chain reaction (PCR). The synovial cells by cocultivation with HTLV-I-infected T cell lines proliferate actively and transform. The proliferation of the synovial cells was essential to the contact with synovial cells and HTLV-I-producing T cell lines. Moreover, HTLV-I-infected synovial cells produced a significant amount of granulocyte macrophage-colony … More stimulating factor (GM-CSF). These results suggest that HTLV-l may cause chronic inflammetory arthropathy, as similar to that found in rheumatoid arthritis.2. Transfection of HTLV-L pX gene into U937 cells.U937 cells were transfected HTLV-L pX gene using DEAE dextran methods. U937 cells transfected HTLV-L pX gene was detected the pX MRNA by northern blotting and Tax protein by western blotting. A-IT-2 cells expressed the IL-2 Ra mRNA, but transfected U937 cells did not. However, the transfected U937 cells were detected c-fgr mRNA and p58^<c-fgr>.3. Different B-cell responses to human T-cell lymphotropic virus Type I (HTLV-I) envelope synthetic peptides in HTLV-I-infected individuals.We studied the difference in antibody activities against the viral protein and the difference in specificites of anti-HTLV-I envelope antibodies among HTLV-I-infected individuals from the same HTLV-I endemic area using a HTLV-I-gag hybrid protein and HTLV-I-env-encoded synthetic peptides as antigens, respectively. Patients with HTLV-I-infected polyarthritis made antibodies specific for VlE1 (residues 342-363) and VIE8 (191-209). Patients with HTLV-I associated myelopathy (HAM) made antibodies to the VIE7 (97-111) and VIE9 (268-286) epitopes. The activities of anti-HTLV-I antibodies in sera from HTLV-I-infected polyarthritis patients were not different from the activities of the antibodies from normal HTLV-I-carries, and no envelope peptide-specificity unique for the arthritis patients was detected. Less