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Efineptakin alfa (NT-I7) improves overall survival and induces tertiary lymphoid structures in murine lung tumors
Abstract:
Tertiary lymphoid structures (TLSs) are emerging as good predictive biomarkers of response to cancer immunotherapy. However, therapeutic strategies to induce these structures are currently limited. We evaluated the therapeutic benefit of efineptakin alfa (NT-I7), a long-acting form of IL-7, and its ability to induce TLSs in a murine lung tumor model. NT-I7 improved overall survival in tumor-bearing mice. It also increased the abundance of T, B, dendritic cells, and stem-like CD8 T cells and promoted the formation of immune aggregates in the tumor microenvironment (TME). Stem-like CD8 T cells were preferentially located in the immune aggregates. Spatial transcriptomic analyses of the TME further demonstrated that the immune aggregates induced by NT-I7 included TLSs with enrichment of Cd274 (PD-L1) transcripts and genes involved in antigen processing and presentation. Upregulation of Cd274 in the TLSs may provide opportunities for synergy between NT-I7 and PD-1-targeted immunotherapy.
Statement Of Significance:
This study demonstrates the ability of efineptakin alfa (NT-I7) to potentially augment the clinical efficacy of cancer immunotherapy by inducing tertiary lymphoid structures in the tumor microenvironment.
Insights
Efineptakin alfa (NT-I7), a form of IL-7, boosts survival in mice with lung tumors by creating tertiary lymphoid structures (TLSs). These structures enhance anti-cancer immune responses, potentially improving immunotherapy effectiveness.
Area of Science:
- Immunology
- Cancer Research
- Pharmacology
Background:
- Tertiary lymphoid structures (TLSs) are crucial biomarkers for cancer immunotherapy response.
- Current therapeutic strategies to induce TLSs are limited.
- Interleukin-7 (IL-7) plays a role in T-cell homeostasis and immune responses.
Purpose of the Study:
- To evaluate the therapeutic potential of efineptakin alfa (NT-I7), a long-acting IL-7, in a murine lung tumor model.
- To investigate NT-I7's ability to induce TLSs within the tumor microenvironment (TME).
- To explore the impact of NT-I7 on immune cell populations and their spatial organization.
Main Methods:
- Administration of efineptakin alfa (NT-I7) to tumor-bearing mice.
- Assessment of overall survival and immune cell infiltration (T cells, B cells, dendritic cells, CD8 T cells).
- Spatial transcriptomic analysis of the tumor microenvironment to characterize induced immune aggregates and TLSs.
Main Results:
- NT-I7 significantly improved overall survival in tumor-bearing mice.
- NT-I7 treatment increased T, B, dendritic cells, and stem-like CD8 T cells in the TME.
- Induced immune aggregates, identified as TLSs, were enriched for PD-L1 and antigen processing/presentation genes.
Conclusions:
- Efineptakin alfa (NT-I7) demonstrates therapeutic benefit by inducing TLSs in the TME.
- NT-I7 has the potential to augment clinical efficacy of cancer immunotherapy.
- Upregulation of PD-L1 in NT-I7-induced TLSs suggests synergy with PD-1 targeted therapies.
