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FASLG — IL12B

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• STRING interaction: FASLG — IL12B (interaction, mapped from kegg_pathways)
• STRING interaction: IL12B — FASLG (interaction, mapped from kegg_pathways)

Text-mined interactions from Literome

Arnold et al., J Immunol 1999 : Stimulation of the cells with IL-6, IL-10, IL-12 , TGF-beta1, and GM-CSF did not modulate the constitutive FasL expression, but IFN-gamma mediated FasL up-regulation was significantly diminished by IL-10 and TGF-beta1, respectively
Leite-de-Moraes et al., J Immunol 2000 : This process was preceded by up-regulation of Fas ( CD95 ) and Fas ligand expression in response to IL-12 plus IL-18 and was blocked by zVAD, a large spectrum caspase inhibitor, as well as by anti-Fas ligand mAb, suggesting the involvement of the Fas pathway
Kitaura et al., J Immunol 2002 : In contrast, IL-12 induced FasL transcription to lead to FasL expression on the surfaces of nonadherent bone marrow cells, whereas TNF-alpha could not induce FasL on the cells ... These results implied that apoptosis of the adherent cells in bone marrow cells might be caused by interaction between TNF-alpha induced Fas on the adherent cells and IL-12 induced FasL on the nonadherent cells
Kidoya et al., J Immunol 2005 (Inflammation) : Fas ligand induces cell-autonomous IL-23 production in dendritic cells, a mechanism for Fas ligand induced IL-17 production ... FasL induced the production of IL-23 in PEC in vivo and in vitro, and IL-17 production following the i.p. injection of FFL cells was severely impaired in p40-/- mice, indicating that IL-23 plays an important role in the FasL induced IL-17 production ... Finally, FasL induced only weak p40 production in a mixture of p40-/- and Fas-/- DC, indicating that FasL induces IL-23 production in DC mainly in a cell-autonomous manner
Kitaura et al., Immunol Lett 2006 : We previously reported that the proinflammatory cytokine IL-12 induced apoptosis in TNF-alpha mediated osteoclastogenesis in mouse bone marrow culture through an interaction of Fas and Fas ligand (FasL) ... Furthermore, IL-18 and IL-12 synergistically induced apoptosis of adherent bone marrow cells in the presence of TNF-alpha, and up-regulated FasL transcription in non-adherent cells
Matsuda et al., Int J Oncol 2006 (Disease Models, Animal...) : We found that mAb treatment activates Kupffer cells to produce inflammatory cytokines such as TNF-alpha and IL-12 , and induces the expression of FasL on Kupffer and NKT cells
Reay et al., Cancer Gene Ther 2009 (Fibrosarcoma) : In addition, we have shown that the antitumor activity of IL-23 is independent of IL-17, perforin and Fas ligand , but dependent on interferon-gamma, CD4 ( + ) and CD8 ( + ) T cells
Yoshimatsu et al., Bone 2009 : We previously reported that IL-12 induces apoptosis in bone marrow cells treated with TNF-alpha in vitro via an interaction between TNF-alpha induced Fas and IL-12 induced Fas ligand (FasL) , and that, as a result, osteoclastogenesis is inhibited ... These results suggest that IL-12 inhibits TNF-alpha mediated osteoclastogenesis and induces apoptotic changes through an interaction between TNF-alpha induced Fas and IL-12 induced FasL , in vivo, via a T cell independent mechanism
Kondo et al., Immunology 2009 (Myositis) : Taken together, these results suggest that proinflammatory cytokines enhance Fas mediated apoptosis of muscle cells, and that the Fas/FasL interaction between invading dendritic cells and CD4 ( + ) T cells induces local production of IL-23 and proinflammatory cytokines, which can promote the proliferation of Th17 cells and enhance Fas mediated apoptosis of muscle cells, respectively
Hu et al., Mol Med Report 2008 : SOCS1 silencing in DCs could prevent immune tolerance by inhibiting Fas and Fas-L expression, induced by an increase in IL-12p70 and IL-6 production
Kitaura et al., Calcif Tissue Int 2011 : We have reported that IL-12 and IL-18 induce apoptosis in bone marrow cells treated with TNF-a in vitro and that osteoclastogenesis is inhibited by the interaction of TNF-a induced Fas and the IL-12 induced Fas ligand (FasL)
Kitaura et al., Clin Dev Immunol 2013 (Arthritis, Rheumatoid...) : IL-12, IL-18, and IFN- ? induce apoptosis in bone marrow cells treated with TNF- a ??in vitro, and osteoclastogenesis is inhibited by the interactions of TNF- a -induced Fas and Fas ligand induced by IL-12 , IL-18, and IFN- ?