GILZ (F2U9K) Rabbit Monoclonal Antibody #25841

Glucocorticoids (GCs) are drugs with potent anti-inflammatory and immunosuppressive effects. GCs act by inhibiting the function of macrophages and antigen-presenting cells (1,2), and their varied biological effects are controlled by several well-characterized pathways (3-5). Identifying proteins that are transcriptionally regulated downstream of GC treatment is of significant research interest. Glucocorticoid-induced leucine zipper (GILZ), also known as TSC22 domain family member 3 (TSC22D3), is a protein primarily expressed under glucocorticoid receptor (GR) transcriptional control. GILZ was first identified in a screen for genes mediating GC-induced apoptosis (3). GILZ has subsequently been shown to regulate apoptosis, proliferation, and differentiation, in addition to signaling pathways associated with host immunity and inflammation (4,5). One mechanism by which GCs induce immunosuppression is through regulation of the T cell response (1,5). GILZ interferes with the function of AP-1 and NF-κB in T lymphocytes and macrophages (2,4). GILZ also inhibits NF-κB by directly binding to the p65 subunit, preventing its interaction with specific gene regulatory elements (3). Recent research has focused on the role of GILZ in stress response and tumor biology (6-8). GILZ expression is associated with poor prognosis in patients with acute myeloid leukemia (AML) and is being investigated as a prognostic biomarker (7). Furthermore, combined therapy targeting GILZ alongside PD-L1 checkpoint blockade has been shown as an effective method to prevent immune escape in glioblastomas (8).