ChIP-seq for PPARg, RXRa, and H3K27Ac in inflammation-associated unsaturated fatty acid-supplemented Th2 cells

A unique subpopulation of memory Th2 cells expressing the interleukin-33 receptor ST2 contributes to the pathogenesis of allergic diseases; however, the immune-metabolic mechanisms that induce ST2hi memory Th2 cells in inflamed tissues remain uncertain. We revealed that linoleic and oleic acids increased in the inflamed lungs induced ST2 expression through activating PPARg. Furthermore, this activation of PPARg was dependent on ATGL activity. Overall design: Each fatty acid complexed to BSA was added to the cell culture medium at a final concentration of 20 µM during the differentiation of Th2 cells from splenic naïve CD4+ T cells. Cells were treated with DMSO or ATGL inhibitor atglistatin (15 µM in DMSO; Sigma-Aldrich) were added to the cell culture medium from day 4. ChIP-seq were conducted on day 5.