Gene interactions and pathways from curated databases and text-mining

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FASLG — IL4

Text-mined interactions from Literome

Aung et al., J Immunol 2000 (Leukemia L1210) : Analysis of FasL expression by flow cytometry showed that IL-4 increased cell surface FasL expression on CD4+ and CD8+ splenocytes, with peak expression on day 4 after infection
Lundy et al., Infect Immun 2002 (Schistosomiasis mansoni) : These results suggest that FasL expressing, splenic B-1a cells are important mediators of SEA stimulated CD4 ( + ) -T-cell apoptosis and that maximal FasL expression on B-1a cells is dependent on antigenic stimulation and the presence of IL-4 and IL-10
Acosta Rodriguez et al., J Leukoc Biol 2003 (Chagas Disease) : It is interesting that the protective effect of IL-4 over B cells from infected mice is mediated , at least partly, by the down-regulation of Fas ligand (FasL) expression, which leads to interference in the apoptosis executed by these B cells through the Fas/FasL death pathway ... Accordingly, a marked up-regulation of the `` FasL gene repressor '' class II transactivator was observed, suggesting that this would be one mechanism underlying the IL-4 mediated FasL down-regulation
Duan et al., Clin Cancer Res 2004 (Osteosarcoma) : The purpose of these studies was to determine whether alkylating agents affect the expression of Fas ligand (FasL) and whether interleukin 12 enhances the sensitivity of human OS cells to alkylating agents
Guillermo et al., J Leukoc Biol 2007 (Chagas Disease) : Anti-FasL , but not anti-TNF-alpha or anti-TRAIL, blocked activation induced cell death of CD8 T cells and increased secretion of IL-10 and IL-4 by CD4 T cells from T. cruzi infected mice
Chakour et al., J Leukoc Biol 2009 : These results show that FasL synergizes with IFN-gamma to activate macrophages and that the tight regulation by IFN-gamma and/or IL-4 of the nonapoptotic signaling events triggered by the Fas-FasL pathway affects significantly the activation of macrophages to a microbicidal state and may thus contribute to the pathogenesis of L. major infection