TNF-α/IL-17 synergy inhibits IL-13 bioactivity via IL-13Rα2 induction

TNF-α/IL-17 synergy inhibits IL-13 bioactivity via IL-13Rα2 induction.

IL-13 signaling via IL-13Rα2 triggers TGF-β1-dependent allograft fibrosis

BACKGROUND Allograft fibrosis still remains a critical problem in transplantation, including heart transplantation. The IL-13/TGF-β1 interaction has previously been identified as a key pathway orchestrating fibrosis in different inflammatory immune disorders. Here we investigate if this pathway is also responsible for allograft fibrosis and if interference with the IL-13/TGF-β1 interaction prev...

Silencing IL-13Rα2 promotes glioblastoma cell death via endogenous signaling.

Glioblastoma multiforme (GBM) is one of the most lethal forms of cancer, with a survival rate of only 13% to 27% within 2 years of diagnosis despite optimal medical treatment. We hypothesize that the presence of a unique IL-13Rα2 decoy receptor prevents GBM apoptosis. This receptor has a high affinity for interleukin-13 (IL-13), binds the cytokine, and competitively inhibits the intracellular s...

Cytoplasmic tail of IL-13Rα2 regulates IL-4 signal transduction

IL (interleukin)-4 and IL-13 are key cytokines in the pathogenesis of allergic inflammatory disease. IL-4 and IL-13 share many functional properties as a result of their utilization of a common receptor complex comprising IL-13Rα1 (IL-13 receptor α-chain 1) and IL-4Rα. The second IL-13R (IL-13 receptor) has been identified, namely IL-13Rα2. This has been thought to be a decoy receptor due to it...

Synergistic induction of eotaxin expression in human keratocytes by TNF-alpha and IL-4 or IL-13.

PURPOSE To investigate the effects of tumor necrosis factor (TNF)-alpha, interleukin (IL)4, and IL-13 on expression of the chemokine eotaxin by cultured human keratocytes. METHODS Cultured human keratocytes were incubated with various combinations and concentrations of TNF-alpha, IL-4, and IL-13. The concentration of eotaxin in the culture supernatant was subsequently measured by enzyme-linke...