The interleukin-7 receptor (IL7R), composed of the IL7Rα (CD127) and common γ-chain (γc), plays a critical role in lymphocyte development, homeostasis, and immune regulation. Dysregulation of IL7R signaling is implicated in autoimmune diseases (e.g., multiple sclerosis, rheumatoid arthritis), hematologic malignancies (e.g., acute lymphoblastic leukemia), and inflammatory disorders. IL7R-targeting antibodies have emerged as therapeutic tools to modulate this pathway.
Current research focuses on blocking IL7R to suppress pathogenic T-cell activity in autoimmunity or disrupt survival signals in cancer cells. For example, anti-IL7Rα antibodies have shown preclinical efficacy in reducing disease severity in experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. Conversely, in T-cell acute lymphoblastic leukemia (T-ALL), IL7R overexpression drives oncogenic signaling, making it a potential target for antibody-mediated inhibition.
Challenges include balancing therapeutic effects with potential immunosuppression risks, as IL7R is essential for normal immune function. Novel strategies like antagonistic antibodies, bispecific designs, or combination therapies aim to enhance specificity. Several candidates are in early-stage clinical trials, though none have yet reached approval. Understanding IL7R's dual roles in immunity and disease continues to guide antibody engineering for safer, more precise interventions.