PD-1 is induced by toll-like receptor signaling on mouse splenic DCs and negatively regulates function of DC cells during Listeria infection.[21] In ovarian cancer patients, PD-1 was co-expressed with PD-L1 on tumor-infiltrating DC (TIDC) cells and blunted TIDC function by inactivating the NF-kb pathway.[22] Expression of PD-1 on NK cells limits their function and PD-1 blockade restores NK cell anti-tumor function.[23] ILC2 cells from adipose tissue of obese mice also upregulate PD-1 in a manner that depends on TNF and IL-33. This evidence concerns the gene IL33 and neoplasm.