Expansion of PMN-myeloid derived suppressor cells and their clinical relevance in patients with oral squamous cell carcinoma.

OBJECTIVES: Oral squamous cell carcinoma (OSCC) is the most common head and neck malignancy worldwide, with a high mortality. The prognosis of OSCC remains unsatisfactory; the dysregulated immune system plays an important role in the pathogenesis of OSCC. Myeloid-derived suppressor cells (MDSCs) have been identified as immune-suppressive cells in multiple tumor types. The aim of this study was to clarify the underlying immunoregulatory mechanism of MDSC in patients with OSCC. MATERIALS AND METHODS: Flow cytometry was used to analyze the phenotype of MDSC among peripheral blood mononuclear cells (PBMCs) from patients with OSCC and healthy control subjects. The correlation between MDSC frequency and the disease index of patients with OSCC was evaluated. T cell proliferation experiment was used to evaluate the immunosuppressive function of MDSC. RESULTS: Patients with OSCC exhibited significantly higher levels of PMN-MDSCs than did healthy controls. In the co-culture assay, T cell proliferation and IFN-γ production were abrogated by the addition of PMN-MDSCs in a dose-dependent manner. The levels of reactive oxygen species were higher for PMN-MDSCs derived from patients with OSCC than for those from normal individuals. p-STAT3 levels, a key activator of MDSCs, was higher in OSCC-related PMN-MDSCs than in those from healthy controls. Both of these effects were reversed by NAC (an ROS inhibitor) and JSI-124 (a p-STAT3 inhibitor). Finally, PMN-MDSC levels were positively related to histological differentiation, nodal metastasis, and recurrence. CONCLUSION: PMN-MDSCs were elevated in OSCC patients, with strong immune-suppressive effects via p-STAT3/reactive oxygen species, providing a new direction for therapeutic strategies.

A humoral immunity survey following the 2012 influenza season after the pH1N1 pandemic in Guangzhou, China.

According to pathogenic surveillance data during the first half of 2012, the H3N2 influenza virus was prevalent in Guangdong, China, but no pandemic H1N1 (pH1N1) virus was detected. This study aimed to measure the seroprevalence of pH1N1 and H3N2 infection following the influenza epidemic in 2012. We collected serum samples by stratified random sampling in a cross-sectional survey from August, 2012 to October, 2012. Antibody titers against H3N2, pH1N1, and influenza B antigens were measured by the hemagglutination inhibition (HI) assay, and age-specific seroprevalence and non-immunity were calculated. A total of 566 serum samples were collected from subjects who had not received an influenza vaccination. The seroprevalence of H3N2, pH1N1, and influenza B were 61.7%, 31.3%, and 40.4%, respectively, while non-immunity was calculated to be 9.2%, 40.6%, and 27.0%, respectively. The highest recorded seroprevalence was 86.0% for H3N2 in the 6-15 year age group, while the lowest was 14.6% for pH1N1 in the 60+ age group. Non-immunity fractions were 44.4% and 53.5% in the 0-6 and 60+ age groups, respectively. In conclusion, the seroprevalence of pH1N1 remained below 50% in all age groups following the 2012 influenza season. These data suggest that vaccination against pH1N1 antigens should be conducted, especially in the older age groups, before the next influenza season.

Amniotic stem cell transplantation therapy for type 1 diabetes: a case report.

This case report presents an evaluation of the clinical effects of an allogeneic amniotic cell transplant for the treatment of type 1 diabetes mellitus. A 26-year-old man with type 1 diabetes was treated with stem cells isolated from his neonatal son's amniotic membrane, collected at birth (2 × 10(7) cells). The cells, which expressed high levels of cluster of differentiation (CD) 133 and CD34 as assessed by flow cytometry, were infused into the pancreatic dorsal artery through the left femoral artery. The main study outcome was the change in exogenous insulin requirements, which began to decrease 3 days after transplantation. At 3 months post-transplantation, the patient was insulin independent and remained so for 6.2 months. During a 36-month follow-up, the patient's blood glucose remained under control and insulin treatment was readjusted to a dosage of 8 IU/day. These preliminary data suggest that amniotic membrane stem cell transplantation can improve islet-cell function in response to glucose in vivo, although an alternative explanation (such as a honeymoon period due to reduced glucose toxicity) also has to be considered.

[Effect of small interfering RNA-mediated silencing of CD158b expression on the cytotoxicity of NK cells against the allogeneic dendritic cells].

OBJECTIVE: To study the effects of small interfering RNA (siRNA)-mediated silencing of CD158b expression on the efficiency of the natural killer (NK) cells in killing allogeneic dendritic cells. METHODS: After the knockdown of CD158b by CD158b -SiRNA, the CD158b mRNA expression in natural killer cells was examined by qRT-PCR and the CD158b protein expression by flow cytometer. The cytotoxic activity of RNAi-NK cells and normal NK cells against the allogeneic dendritic cells was detected by LDH release assay. RESULTS: The CD158b mRNA expression and its protein expression were decreased significantly in the NK cells by CD158b siRNA (P/0.05). The cytotoxic activities of alloreactive NK cells generated by RNAi CD158b expression against allogeneic dendritic cells were increased significantly. CONCLUSION: Silencing CD158b gene can inhibit the NK cell CD158B mRNA and protein expression. Alloreactive NK cells generated by RNAi CD158b expression have the potential for use in interventions of GVHD.

[In vitro proliferation of CD4(+)CD25(+) T cells from PBMCs of the chronic myelocytic leukemia patients and their inhibitory effect on CD4(+)CD25(-) T cells].

OBJECTIVE: To investigate the in vitro proliferation of CD4(+)CD25(+) T cells from the peripheral blood mononuclear cells (PBMCs) of the chronic myelocytic leukemia patients and the inhibitory effect on CD4(+)CD25(-) T cells. METHODS: Magnetic-activated cell sorting (MACS) was used to separate CD4(+)CD25(+) T and CD4(+)CD25(-) T cells from the PBMCs of patients with chronic myelocytic leukemia, and the purity and activity of CD4(+)CD25(+) T cells were analyzed with flow cytometry. After stimulation with anti-CD3 mAb, anti-CD28 mAb and recombinant human interleukin-2 (rhIL-2), the CD4(+)CD25(-) and CD4(+)CD25(+) T cells were cocultured to observe the inhibitory effect of CD4(+)CD25(+)T on CD4(+)CD25(-)T cells using MTT assay. RESULTS: After cell sorting, the purity of CD4(+)CD25(+)T cells from healthy control and chronic myelocytic leukemia patients were (84.93-/+2.55)% and (86.32-/+2.40)%, respectively, showing no significant difference between them (P>0.05). The activity of CD4(+)CD25(+) and CD4(+)CD25(-) T cells from healthy control and the leukemic patients was also comparable [(98.12-/+0.68)% vs (97.33-/+0.78)%, P>0.05). In the coculture, CD4(+)CD25(+) T cells obviously inhibited CD4(+)CD25(-) T cell proliferation in vitro, and the maximum inhibition occurred when CD4(+)CD25(+)T cells were cocultured with CD4(+)CD25(-)T cells at the ratio of 1:1. CONCLUSION: The MACS system can effectively isolate CD4(+)CD25(+) and CD4(+)CD25(-) T cells. CD4(+)CD25(+) T cells obviously inhibit the proliferation of CD4(+)CD25(-)T cells in vitro, and the effect displays an effector-target ratio relationship.

[Effects of basic fibroblast growth factor on rat models of Alzheimer disease].

OBJECTIVE: To study the effects of basic fibroblast growth factor (bFGF) on the praxiology and cerebral acetylcholinesterase (AchE) fiber density of kainic acid-lesioned rat models of Alzheimer disease (AD). METHODS: AD models were induced in 30 normal adult rats by damaging the rat nucleus basalis of Meynert (NBM) with kainic acid, and the models were then assigned into 3 groups to receive cerebroventricular infusion with bFGF, saline or nothing for treatment, serving respectively as the treatment group at 30 min, 1, 3 and 7 d after the injury, sham treatment group or injury group. Another 10 rats were used as control group, which received saline injections into the NBM without further treatment. The learning and memory abilities of the rats were measured through Y-maze test 30 d after the operations, and AchE cytochemical study was conducted to calculate the density of the AchE fibers in the hippocampus and forebrain of the rats. RESULTS: In comparison with the injury group, improvement was noted in the memory ability of rats with bFGF treatment and the density of AchE fiber was also significantly increased (P<0.01), but the improvement in both respects failed to reach the normal level (P<0.01). CONCLUSIONS: AD model can be successfully established by damaging the NBM with kainic acid, and bFGF is beneficial in improving the impaired learning and memory abilities and increasing the density of AchE fibers in the basal forebrain cortex and hippocampus in the models.