Objective To study the production and distribution of vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein 1 (MCP-1) in the skin and sera of patients with psoriasis and their roles in the pathogenesis of psoriasis. Methods Levels of VEGF and MCP-1 in sera were measured using double antibody sandwich enzyme linked immunosorbent assay(ELISA) in patients with psoriasis. The expression and distribution of VEGF and MCP-1 in psoriatic lesions, non lesional skin and normal controls were detected by immunohistochemical method. Results ①The expression of VEGF in lesional skin and non lesional skin of psoriasis patients was higher than that in normal controls. Levels of MCP-1 were increased in lesional skin than those in non lesional skin and normal controls.②Serum levels of VEGF were significantly increased in psoriasis as compared with normal control. There was no significant difference in serum levels of MCP-1 between patients and controls.③There was no correlation between the expression of MCP-1 or VEGF of psoriatic lesion and PASI index. Conclusion Overexpression of two cytokines, VEGF and MCP-1, known to promote new blood vessel formation may contribute to the pathogenesis of psoriasis.

Objective To understand the molecular mechanism underlying the epidermal growth factor receptors(EGFR)signal transduction and its feed-back regulation.Methods Two human keratinocyte cell lines,HaCaT and CHOwt,were cultured and treated with a certain concentration of different ligands,including epidermal growth factor(EGF),heparin-bounding(HB)-EGF,transforming growth factor α (TGFα)and heregulin(HER),for various durations(2,4,8,16,20 hours).After the treatment,cells were collected and protein was extracted.The amount of total and active EGFR was measured by immunoprecipitation and immunoblot assay.The internalization and down-regulation of EGFR were visualized with immunofluorescence and laser seanning confocal microscopy.Results As shown by immunoblot technique,EGF and HB-EGF continuously down-regulated the total amount of EGFRs,whereas TGFα and HER had no significant effect on the degradation of EGFRs.The activation of EGFRs was also attenuated to different extent after long-time treatment with EGF,HB-EGF and TGFα.As indirect immunofluorescenee revealed,in untreated HaCaT and CHOwt cells,EGFRs were essentially located at the plasma membrane,with a little cytosolic distribution;after ten-minute treatment with EGF,EGFRs clustered into patch-like structures which were particularly obvious in HaCaT cells,and translocated into cytoplasmic vesicles resembling endosomes (relatively apparent in CHOwt cells),while the total amount of EGFRs remained constant in these cells.The fluorescence signal from the total EGFRs decreased evidently after four-hour treatment with EGF,indicating a strong reduction in the receptors.Conclusions EGF and HB-EGF,but not TGFα or Heregulin,could down-regulate the amount of total and active EGFRs.There might be different mechanisms for the signal transduction related to EGFRs intemalization and down-regulation between HaCaT and CHOwt cells.

Objective To determine the relationship between serum levels of MCAF/MCP-1 (monocyte chemotactic and activating factor/monocyte chemoattractant protein-1), RANTES(regulated on activation, normal T-cell expressed and secreted) and the disease activity of systemic lupus erythematosus(SLE). Methods Serum levels of MCAF and RANTES were measured by ELISA. Results ①Serum level of MCAF but not RANTES, was significantly increased in patients with SLE as compared with controls. ②Serum level of MCAF but not RANTES, was markedly higher in patients with active disease than those with inactive disease. ③No significant differences were found in the serum levels of MCAF and RANTES between patients with renal damage and those without. Conclusions These results suggest that MCAF may be involved in the pathogenesis of SLE, and serum MCAF levels could be an indicator for the disease activity of SLE.

Despite exciting achievements with some malignancies, immunotherapy for hypoimmunogenic cancers, especially glioblastoma (GBM), remains a formidable clinical challenge. Poor immunogenicity and deficient immune infiltrates are two major limitations to an effective cancer-specific immune response. Herein, we propose that an injectable signal-amplifying nanocomposite/hydrogel system consisting of granulocyte-macrophage colony-stimulating factor and imiquimod-loaded antigen-capturing nanoparticles can simultaneously amplify the chemotactic signal of antigen-presenting cells and the "danger" signal of GBM. We demonstrated the feasibility of this strategy in two scenarios of GBM. In the first scenario, we showed that this simultaneous amplification system, in conjunction with local chemotherapy, enhanced both the immunogenicity and immune infiltrates in a recurrent GBM model; thus, ultimately making a cold GBM hot and suppressing postoperative relapse. Encouraged by excellent efficacy, we further exploited this signal-amplifying system to improve the efficiency of vaccine lysate in the treatment of refractory multiple GBM, a disease with limited clinical treatment options. In general, this biomaterial-based immune signal amplification system represents a unique approach to restore GBM-specific immunity and may provide a beneficial preliminary treatment for other clinically refractory malignancies.