ArticleJournal of experimental & clinical cancer research : CR2026
PD1-IL2v expands and induces effector CD8
Article in Journal of experimental & clinical cancer research : CR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe combination of systemic immune checkpoint inhibitors with standard of care intravesical Bacillus Calmette-Guerin (BCG) therapy for non-muscle invasive bladder cancer (NMIBC) has shown potential in enhancing BCG therapeutic effects. However, challenges such as disease recurrence, progression, and immune-related toxicities remain a significant hurdle. Furthermore, the mechanism of action of BCG involves broad, non-specific immune activation. While this recruits bystander CD8+ and NK cells, it also triggers the undesired expansion of Tregs, which may ultimately hamper therapeutic efficacy. We aimed to explore the feasibility of a targeted approach designed to overcome intravesical tumor resistance and selectively enhance the expansion and effector functions of CD8+ TILs.
methodsWe tested intravesical administration of BCG with murinized PD1-IL2v, a fusion protein that simultaneously targets PD-1 and IL-2Rβγ in cis on the same cell, in a preclinical mouse model of NMIBC.
resultsBoth BCG monotherapy and co-treatment with a murinized PD1-IL2v improved animal survival. Notably, the intravesical combination of BCG and murinized PD1-IL2v significantly increased the number of CD8+ TILs with polyfunctional cytotoxic effector phenotype and avoided Treg expansion in contrast to BCG monotherapy. In addition, in patient-derived tumors, we observed a higher frequency of CD8⁺ TILs (18%) compared to Tregs (5%), with 60% of the CD8+ TILs expressing PD-1 on their surface, representing a potential target for PD1-IL2v, alias eciskafusp alfa.
conclusionsThe intravesical combination of BCG with murinized PD1-IL2v selectively increases the number of cytotoxic CD8+ TILs, but not Tregs, and improves the survival of the mice in the preclinical model of bladder cancer model. These findings support the rationale for exploring the clinical use of eciskafusp alfa for intravesical administration in high-risk NMIBC patients. The combination of BCG and eciskafusp alfa could be deployable as a second line of treatment for NMIBC patients unresponsive to BCG.
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