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Cotargeting TREM2 and IL2 pathways triggers multipronged anticancer immunity.

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A novel antibody fusion, MiTE-144, targets TREM2 (triggering receptor expressed on myeloid cells 2) on tumor cells. This approach shows improved anti-cancer effects and reduced side effects compared to existing therapies.

Keywords:
cancer immunotherapyimmunocytokinesmyeloid checkpointstumour‐associated macrophages

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Area of Science:

  • Immunology
  • Oncology
  • Cancer Research

Background:

  • Triggering receptor expressed on myeloid cells 2 (TREM2) is a key immunosuppressive target on tumor-associated macrophages (TAMs) within the tumor microenvironment (TME).
  • Therapeutic TREM2 blockade has shown suboptimal efficacy in cancer patients.
  • Existing immunotherapies like IL2-based approaches can cause systemic inflammation and hepatotoxicity.

Purpose of the Study:

  • To evaluate the efficacy of a novel antibody fusion, MiTE-144, combining TREM2 blockade with TME-restricted IL2 activation.
  • To compare the anti-cancer efficiency and safety profile of MiTE-144 against TREM2 blockade alone and generic IL2 immunocytokines.
  • To investigate the impact of MiTE-144 on myeloid cell reprogramming and immune cell activation within the TME.

Main Methods:

  • Development of MiTE-144, a fusion protein comprising a TREM2 blocking antibody and an IL2 variant with TME-restricted activation.
  • Preclinical testing of MiTE-144 in cancer models.
  • Assessment of anti-cancer efficacy, systemic inflammation, and hepatotoxicity.
  • Detailed analysis of the tumor microenvironment (TME) post-treatment, including myeloid compartment reprogramming and immune cell activation (NK/CD8+ T cells).

Main Results:

  • MiTE-144 demonstrated superior anti-cancer efficiency compared to TREM2 blockade alone in preclinical settings.
  • MiTE-144 exhibited reduced systemic inflammation and hepatotoxicity relative to TREM2 blockade and generic IL2 immunocytokines.
  • Treatment with MiTE-144 led to significant reprogramming of myeloid compartments and activation of NK/CD8+ T cells within the TME.

Conclusions:

  • MiTE-144 represents a promising therapeutic strategy that overcomes limitations of anti-TREM2 monotherapy.
  • The TME-restricted IL2 activation enhances anti-cancer efficacy while mitigating systemic toxicity.
  • Further research is needed to address immunotherapy barriers in therapy-refractory tumors.