Overview
- In mouse models, a dimeric IgA monoclonal antibody traversed epithelial layers into kidney cysts by engaging polymeric immunoglobulin receptors.
- The antibody antagonized the cMET receptor, reducing downstream growth signaling implicated in polycystic kidney disease progression.
- Treatment triggered apoptosis in cyst-lining cells while sparing healthy renal tissue, with no apparent deleterious effects reported.
- The team converted an IgG backbone into a dIgA format through DNA sequence engineering, verified target engagement in vitro, and observed cyst entry and retention in vivo.
- Authors highlight the need to compare additional growth-factor targets, explore antibody combinations, and secure partners and manufacturing capacity, noting NIH and U.S. Department of Defense support.