Gilead Sciences announced on its third-quarter earnings call Oct. | Gilead Sciences announced on its third-quarter earnings call Oct. 29 that the company has placed a partial clinical hold on two…

Bispecific PD-L1×4-1BB antibodies under clinical development enhance antitumor T cell responses. Luri-Rey et al. find that the efficacy of PD-L1×4-1BB antibodies relies on PD-L1-expressing type 1 conventional dendritic cells, which integrate antigen cross-presentation, IL-12, and 4-1BB costimulation to promote efficacious T cell-mediated antitumor immunity.

Read the full paper: NKG2D overexpression potentiates CAR-T cells through costimulation by tumor NKG2D ligands

Li et al. show that activated CAR-T cells upregulate NKG2D ligands (NKG2DLs), rendering them susceptible to NK cells. Overexpressing NKG2D shields endogenous ligands and harnesses tumor NKG2DLs for costimulation, thereby enhancing CAR-T cell persistence, tumor infiltration, and antitumor efficacy across multiple models.

Blocking B7 costimulation was expected to dampen microbiota-specific RORγt⁺ Treg cells. Instead, it expanded them. Read Mengze’s own account of the surprise.

Understanding regulation of progenitor exhausted CD8+ T (Tpex) cell differentiation is important for immunotherapies. Humblin et al. report that sustained ICOS costimulation is detrimental to PD-1+CD8...

This AST Communities of Practice webinar is on: "CD38-Targeting Agents Along With Costimulation Blockade in the New Era of Desensitization" - Recorded live on Tuesday, May 27, 2025 - This webinar was…

This AST Communities of Practice webinar is on:"CD38-Targeting Agents Along With Costimulation Blockade in the New Era of Desensitization"- Recorded live on ...

Advantage plans do a better job than standalone Part D policies, albeit with important gaps

ICOS agonists are being investigated for cancer immunotherapy based on the idea that they will reinvigorate exhausted CD8+ T cell anti-cancer immunity. Humblin et al. unexpectedly find the opposite—that CD8+ T cell-intrinsic ICOS expression restrains rather than promotes exhausted CD8+ T cell function in both chronic viral infection and tumor models.

Understanding regulation of progenitor exhausted CD8+ T (Tpex) cell differentiation is important for immunotherapies. Humblin et al. report that sustained ICOS costimulation is detrimental to PD-1+CD8+ T cell responses. Limiting ICOS signaling enhances Tpex cell stemness and differentiation into effector-like cells with improved survival and functionality. ICOSL blockade reinvigorates PD-1+CD8+ T cells and promotes viral or tumor control, potentiating PD-1 targeted immunotherapy.

Understanding regulation of progenitor exhausted CD8+ T (Tpex) cell differentiation is important for immunotherapies. Humblin et al. report that sustained ICOS costimulation is detrimental to PD-1+CD8+ T cell responses. Limiting ICOS signaling enhances Tpex cell stemness and differentiation into effector-like cells with improved survival and functionality. ICOSL blockade reinvigorates PD-1+CD8+ T cells and promotes viral or tumor control, potentiating PD-1 targeted immunotherapy.