| First Author | Tassi I | Year | 2009 |
| Journal | Eur J Immunol | Volume | 39 |
| Issue | 5 | Pages | 1369-78 |
| PubMed ID | 19404984 | Mgi Jnum | J:148087 |
| Mgi Id | MGI:3843529 | Doi | 10.1002/eji.200839313 |
| Citation | Tassi I, et al. (2009) Requirement of phospholipase C-gamma2 (PLCgamma2) for Dectin-1-induced antigen presentation and induction of TH1/TH17 polarization. Eur J Immunol 39(5):1369-78 |
| abstractText | DC recognize microbial components through an array of receptors known as PRR. PRR initiate intracellular signals, which engender DC with the capacity to stimulate T-cell responses. Dectin-1 is a PRR that recognizes beta-glucan, a major constituent of many fungi's outer cell wall. Here we show that Dectin-1 activates DC through phospholipase (PLC)gamma2 signaling. PLCgamma2-deficient DC were unable to expand antigen-specific T cells and induce T(H)1 and T(H)17 differentiation in response to beta-glucan. Mechanistically, PLCgamma2-deficiency impaired the capacity of DC to secrete polarizing cytokines following exposure to beta-glucan. Dectin-1 required PLCgamma2 to activate MAPK, AP-1 and NF-kappaB, which induce cytokine gene expression. Moreover, PLCgamma2 controlled Dectin-1-mediated NFAT activation and induction of NFAT-dependent genes such as IL-2, cyclooxigenase-2 and Egr transcription factors. We conclude that PLCgamma2 is a crucial signaling mediator that modifies DC gene expression program to activate DC responses to beta-glucan-containing pathogens. |
