Tumor immune microenvironment (TIME) to enhance antitumor immunity.

The tumor microenvironment is a result of dynamic interaction between different cellular and non-cellular components. In its essence it is not a solo performer, but an ensemble of performers that includes cancer cells, fibroblasts, myo-fibroblasts, endothelial cells and immune cells. The short review highlights important immune infiltrates within the tumor microenvironment that shape cytotoxic t lymphocyte (CTL)-rich immune hot and CTL-deficient immune cold tumors and novel strategies that have potential role in enhancing our immune responses in both immune hot and immune cold tumors.

[Reactive oxygen species mediate the injury and deficient hematopoietic supportive capacity of umbilical cord derived mesenchymal stem cells induced by iron overload].

Objective: To explore the effects of iron overload on umbilical cord derived mesenchymal stem cells (UC-MSC) and elucidate the involvement of reactive oxygen species (ROS) in this process.

Methods: The iron overload model of MSC was established by in vitro addition of ferric ammonium citrate (FAC) into culture medium. Cell proliferation and apoptosis were determined by Annexin V/PI double staining and population doubling time (DT) respectively.

Free iron catalyzes oxidative damage to hematopoietic cells/mesenchymal stem cells in vitro and suppresses hematopoiesis in iron overload patients.

Objectives: Transfusional iron overload is of major concern in hematological disease. Iron-overload-related dyserythropoiesis and reactive oxygen species (ROS)-related damage to hematopoietic stem cell (HSC) function are major setbacks in treatment for such disorders. We therefore aim to investigate the effect of iron overload on hematopoiesis in the patients and explore the role of ROS in iron-induced oxidative damage in hematopoietic cells and microenvironment in vitro.

[Effects and mechanism on anti-leukemic activity of cytokine-induced killer cells with an endogenous expression of interleukin-21].

Objective: To explore the effects and mechanism on anti-leukemic activity of cytokine inducing killer (CIK) cells with an endogenous expression of interleukin-21 (IL-21).

Methods: Mononuclear cells were isolated from peripheral blood and cultured with cytokines to generate CIK cells. IL-21 lentiviral vector was constructed and used to transfect 293T cells.

[Effect and mechanism of iron-catalyzed oxidative stress on mesenchymal stem cells].

Objective: To explore effect of iron overload on the proliferation and apoptosis of mesenchymal stem cell(MSCs) and the possible mechanism.

Methods: Iron overload model of MSCs was established by adding ferric ammonium citrae (FAC) into the culture medium at different concentrations (100, 200, 400 Μmol/L) and incubated for different lengths of time (12, 24, 48 h). The levels of labile iron pool (LIP) and reactive oxygen species (ROS) were measured to confirm oxidative stress state in the model.

[Effects of humanized interleukin 21 on anti-leukemic activity of cytokine induced killer cells and the mechanism].

Objective: To explore the effects of humanized interleukin 21 (IL-21) on anti-leukemic activity of cytokine induced killer(CIK) cells derived from peripheral blood(PB) and the mechanism.

Methods: Mononuclear cells were separated from peripheral blood and cultured with cytokines to induce CIK cells. Proliferation of CIK cells with or without IL-21 stimulation and their cytotoxic activity against K562 cells was measured by MTT method.