Browsing by Subject "protein induction"

Filter results by typing the first few letters
Now showing 1 - 2 of 2
  • Thumbnail Image
    ItemOpen Access
    Chitosan polysaccharide suppress toll like receptor dependent immune response
    (Turkish Society of Immunology, 2015) Tincer G.; Bayyurt, B.; Arıca, Y.M.; Gürsel İ.
    Objectives: Chitosan is a widely used vaccine or anti-cancer delivery vehicle. In this study, we investigated the immunomodulatory effect of chitosan/pIC nanocomplexes on mouse immune cells. Materials and methods: Proliferative and cytotoxic features of chitosan were tested via CCK-8 assay on RAW 264. 7. IL-1β production was assessed via ELISA from PEC supernatants. TNF-α, and NO induction from chitosan treated RAW cells detected by ELISA and Griess assay, respectively. mRNA message levels of TLRs and cytokines on macrophages in response to chitosan/pIC nanocomplex treatments were evaluated by RT-PCR. Results: Results revealed that chitosan is non-toxic to cells, however, proliferative capacities of macrophages were reduced by chitosan administration. Mouse PECs treated with chitosan, led to NLRP3 dependent inflammasome activation as evidenced by dose-dependent IL-1β secretion. Chitosan/pIC nanocomplexes did not improve immunostimulatory action of pIC on RAW cells, since TNF-α and NO productions remained unaltered. Expression levels of several TLRs, CXCL-16 and IFN-α messages from mouse splenocytes were down regulated in response to chitosan/pIC nanocomplex treatment. Conclusion: Our results revealed that chitosan is an anti-proliferative and inflammasome triggering macromolecule on immune cells. Utilization of chitosan as a carrier system is of concern for immunotherapeutic applications. © 2015 Turkish Journal of Immunology.
  • Thumbnail Image
    ItemOpen Access
    Differential p21 expression after ionizing and UVC radiation in EBV-transformed lymphoblastoid cells
    (2000) Moyret-Lalle, C.; Lalle P.; Pedeux, R.; Guillot, C.; Martel, S.; Magaud J.-P.; Puisieux, A.; Ozturk, M.
    Responses to DNA-damaging agents appear to be coordinated by p53 through transcriptional activation of critical target genes. Among them, p21WAF1 encodes a protein preventing cells from entering S phase. It is not clear whether p53-mediated response varies depending on the type of DNA damage. Here, we have decided to compare the p53-mediated response of EBV-transformed lymphoblasts to ionizing radiation and UVC irradiation. We have shown that these cells respond to ionizing radiation by a cell cycle arrest as expected. Surprisingly they failed to do so after UVC treatment. Accordingly there was no significant induction of p21 protein in UVC exposed cells despite p53 accumulation. Using isogenic EBV-transformed lymphoblastoid cells expressing E6 protein of HPV18, we have demonstrated that there was no evidence of p53-dependent cell cycle arrest after UVC irradiation. These observations suggest that the p53-mediated response to UVC, in contrast to ionizing radiation, was compromised in EBV-transformed cells and might be cell type-dependent.