Abstract

Kaposi sarcoma (KS) remains a significant oncologic complication of HIV infection, particularly in regions with high HIV prevalence. Despite advances in antiretroviral therapy (ART), the incidence of KS remains elevated among HIV-infected individuals, highlighting the need for novel therapeutic approaches. CTLA-4, a key immune checkpoint molecule, plays a crucial role in regulating T cell activation and immune tolerance. Recent studies have implicated dysregulated CTLA-4 signaling in the pathogenesis of KS, suggesting that CTLA-4 blockade may represent a promising therapeutic strategy for this malignancy. In this review, we discuss the role of CTLA-4 in KS pathogenesis, preclinical and clinical evidence supporting CTLA-4 blockade as a therapeutic approach for HIV-associated KS, and potential challenges and future directions in this field.