Autoimmunity and peginterferon therapy for polycythemia vera

Abstract

Peginterferon‑α is useful to treat myeloproliferative neoplasms (MPNs) but can precipitate broad autoimmunity. By promoting beta-cell, thyroid, and systemic immune injury, it can lead to Type 1 diabetes, autoimmune thyroiditis, systemic lupus erythematosus, or Sjögren's syndrome. Onset typically occurs within the first months but may be delayed until after treatment cessation. Type 1 diabetes is usually irreversible and requires lifelong therapy, whereas thyroiditis and lupus more often improve after interferon withdrawal, though autoantibodies frequently persist. In this narrative review, we provide an overview of how peginterferon can induce autoimmunity in genetically susceptible individuals with pre-existing subclinical autoimmunity. Pre-treatment risk assessment, including personal/family history of autoimmune disease and consideration of baseline thyroid function and anti-GAD antibodies in high-risk patients, may identify those at elevated risk for irreversible complications, particularly Type 1 diabetes. Targeted clinical and laboratory monitoring throughout therapy and for 12–24 months post-cessation can enable early detection and appropriate intervention.