GPR65 and colitis: Loss of functional TDAG8 in Tdag8 knock-out mice increases the recruitment of macrophages and neutrophils to the colon and enhances the expression of pro-inflammatory mediators in murine models of acute and chronic colitis, such as the DSS model of colitis, the T cell transfer model [81, 131], or interleukin (IL)-10-deficient animals [102].