EDAR (Ectodysplasin A Receptor) is a cell-surface receptor belonging to the tumor necrosis factor receptor (TNFR) superfamily. It plays a critical role in ectodermal development, regulating the formation of hair follicles, teeth, sweat glands, and other ectodermal-derived tissues during embryogenesis. EDAR signaling, mediated through its ligand ectodysplasin-A (EDA), activates the NF-κB pathway, influencing cell differentiation and survival. Mutations in *EDAR* are linked to hypohidrotic ectodermal dysplasia (HED), a genetic disorder characterized by sparse hair, missing teeth, and impaired sweat gland development.
EDAR antibodies are tools or therapeutic agents targeting this receptor. In research, they are used to study EDAR's function in development, cancer (e.g., breast, lung), and inflammatory conditions. Therapeutically, anti-EDAR antibodies are explored to modulate EDAR signaling—either as agonists to restore function in HED or antagonists to inhibit overactive pathways in cancers or autoimmune diseases. For instance, agonist antibodies mimicking EDA have shown potential in preclinical models to rescue ectodermal defects. Conversely, blocking antibodies may suppress EDAR-driven oncogenic signaling.
Autoantibodies against EDAR are rare but have been reported in autoimmune disorders, though their clinical significance remains unclear. Challenges in EDAR antibody development include ensuring tissue specificity and minimizing off-target effects. Ongoing studies aim to harness EDAR's role in regenerative medicine, particularly for hair or sweat gland regeneration, highlighting its multifaceted therapeutic potential.