| First Author | Gorjestani S | Year | 2011 |
| Journal | J Biol Chem | Volume | 286 |
| Issue | 51 | Pages | 43651-9 |
| PubMed ID | 22041900 | Mgi Jnum | J:178744 |
| Mgi Id | MGI:5300086 | Doi | 10.1074/jbc.M111.307389 |
| Citation | Gorjestani S, et al. (2011) Phospholipase Cgamma2 (PLCgamma2) Is Key Component in Dectin-2 Signaling Pathway, Mediating Anti-fungal Innate Immune Responses. J Biol Chem 286(51):43651-9 |
| abstractText | C-type lectin receptors (CLRs) such as Dectin-2 function as pattern recognition receptors to sense fungal infection. However, the signaling pathways induced by these receptors remain largely unknown. Previous studies suggest that the CLR-induced signaling pathway may utilize similar signaling components as the B cell receptor-induced signaling pathway. Phospholipase Cgamma2 (PLCgamma2) is a key component in B cell receptor signaling, but its role in other signaling pathways has not been fully characterized. Here, we show that PLCgamma2 functions downstream of Dectin-2 in response to the stimulation by the hyphal form of Candida albicans, an opportunistic pathogenic fungus. Using PLCgamma2- and PLCgamma1-deficient macrophages, we found that the lack of PLCgamma2, but not PLCgamma1, impairs cytokine production in response to infection with C. albicans. PLCgamma2 deficiency results in the defective activation of NF-kappaB and MAPK and a significantly reduced production of reactive oxygen species following fungal challenge. In addition, PLCgamma2-deficient mice are defective in clearing C. albicans infection in vivo. Together, these findings demonstrate that PLCgamma2 plays a critical role in CLR-induced signaling pathways, governing antifungal innate immune responses. |
