GPR65 and asthma: Supporting the anti-inflammatory role of TDAG8, this receptor knockout has been reported to exacerbate inflammation in the anti-type II collagen antibody-induced arthritis model, possibly through the changing functions of neutrophils and macrophages [30], and to stimulate bone resorption in ovariectomized mice though a change in osteoclast function [31], although the survival role of TDAG8 in eosinophils augments rather than attenuates lung inflammation in asthma models [12].