| First Author | Tian J | Year | 2011 |
| Journal | Cell Immunol | Volume | 270 |
| Issue | 2 | Pages | 183-7 |
| PubMed ID | 21636079 | Mgi Jnum | J:176752 |
| Mgi Id | MGI:5292607 | Doi | 10.1016/j.cellimm.2011.05.003 |
| Citation | Tian J, et al. (2011) Increased expression of mGITRL on D2SC/1 cells by particulate beta-glucan impairs the suppressive effect of CD4+CD25+ regulatory T cells and enhances the effector T cell proliferation. Cell Immunol 270(2):183-7 |
| abstractText | beta-Glucans have been shown to enhance immune responses for centuries, which contributes to their anti-tumor property. However, their mechanisms of action are still elusive. Dectin-1, the C-type lectin receptor for beta-glucan, is expressed abundantly on dendritic cells (DCs). Activation of DCs via Dectin-1 can lead to the maturation of DC, inducing both innate and adaptive immune responses against tumor development and microbial infection. In this study, we found that particulate yeast-derived beta-glucans could induce the maturation of murine dendritic cell line D2SC/1 cells and increase the expression of mGITRL on D2SC/1 cells via Dectin-1/Syk pathway in a dose dependent manner. Furthermore, we demonstrated that the increased mGITRL on D2SC/1 cells could impair the suppressive activity of CD4(+)CD25(+) regulatory T cells (Tregs) and enhance the proliferation of CD4(+)CD25(-) effector T cells (Teffs). These findings suggest that particulate beta-glucan can be used as immunomodulator to stimulate potent T cell-mediated adaptive immunity while down-regulate immune suppressive activity, leading to a more efficient defense mechanism against tumor development or infectious diseases. |
