Infection with human immunodeficiency virus （HIV） disrupts the balance among yT cell subsets, with increasing Vo1＋ cells and substantial depletion of circulating Vo2＋ cells. Depletion is an indirect effect of HIV ...Infection with human immunodeficiency virus （HIV） disrupts the balance among yT cell subsets, with increasing Vo1＋ cells and substantial depletion of circulating Vo2＋ cells. Depletion is an indirect effect of HIV in CD4-negative Vo2 cells, but is specific for phosphoantigen-responsive subpopulations identified by the Vy2-Jy1.2 （also called Vy9-JyP） T cell receptor rearrangement. The extent of cell loss and recovery is related closely to clinical status, with highest levels of functional V cells present in virus controllers （undetectable viremia in the absence of antiretroviral therapy）. We review the mechanisms and clinical consequences for V cell depletion in HIV disease. We address the question of whether HIV-mediated V cell depletion, despite being an indirect effect of infection, is an important part of the immune evasion strategy for this virus. The important roles for V cells, as effectors and immune regulators, identify key mechanisms affected by HIV and show the strong relationships between V62 cell loss and immunodeficiency disease. This field is moving toward immune therapies based on targeting V cells and we now have clear goals and expectations to Ruide interventional clinical trials.展开更多
[目的]将购自ATCC的ST贴壁细胞通过自主驯化,使其能在甘肃健顺生物科技有限公司(简称健顺生物)自产的无血清培养基CD ST 258中悬浮生长且能稳定传代,在反应器中能高密度生长。[方法]采用高血清贴壁培养转无血清悬浮培养;单因素实验优化...[目的]将购自ATCC的ST贴壁细胞通过自主驯化,使其能在甘肃健顺生物科技有限公司(简称健顺生物)自产的无血清培养基CD ST 258中悬浮生长且能稳定传代,在反应器中能高密度生长。[方法]采用高血清贴壁培养转无血清悬浮培养;单因素实验优化氨基酸、维生素、无机盐等培养基组分;单因素实验优化生物反应器的pH、溶氧和转速三个参数。[结果]悬浮细胞在无血清培养基中传代,72 h细胞密度高于8.0×10^(6)cells/m L;反应器中细胞最高生长密度可达3.0×10^(7)cells/m L。[结论]ST贴壁细胞可驯化为悬浮细胞,能在无血清培养基中稳定传代且在一次性反应器中可高密度生长。展开更多
文摘Infection with human immunodeficiency virus （HIV） disrupts the balance among yT cell subsets, with increasing Vo1＋ cells and substantial depletion of circulating Vo2＋ cells. Depletion is an indirect effect of HIV in CD4-negative Vo2 cells, but is specific for phosphoantigen-responsive subpopulations identified by the Vy2-Jy1.2 （also called Vy9-JyP） T cell receptor rearrangement. The extent of cell loss and recovery is related closely to clinical status, with highest levels of functional V cells present in virus controllers （undetectable viremia in the absence of antiretroviral therapy）. We review the mechanisms and clinical consequences for V cell depletion in HIV disease. We address the question of whether HIV-mediated V cell depletion, despite being an indirect effect of infection, is an important part of the immune evasion strategy for this virus. The important roles for V cells, as effectors and immune regulators, identify key mechanisms affected by HIV and show the strong relationships between V62 cell loss and immunodeficiency disease. This field is moving toward immune therapies based on targeting V cells and we now have clear goals and expectations to Ruide interventional clinical trials.
