GARP releases active TGFβ1 upon the interaction of LAP with the integrin αVβ8 and thereby regulates the bioavailability of TGFβ1.15,16 Active TGFβ1 released by GARP facilitates the development of additional Tregs or T helper 17 (Th17) cells in a paracrine manner and mediates the immunosuppressive capacity of Tregs.13,17 In this study, we report two PID patients with previously undescribed LRRC32 mutations suffering from severe immune dysregulation and exhibiting Treg defects. Here, LRRC32 is linked to pelvic inflammatory disease.