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Tumor Immunotherapy

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Related Experiment Video

Updated: May 17, 2025

Experimental Infection with Listeria monocytogenes as a Model for Studying Host Interferon-γ Responses

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Published on: November 16, 2016

Interleukin-4 modulates type I interferon to augment antitumor immunity.

Hannah V Newnes^1,2, Jesse D Armitage^1,2, Anthony C Buzzai³

¹School of Biomedical Sciences, The University of Western Australia, Perth, Australia.

Science Advances

|May 14, 2025

Summary

This summary is machine-generated.

Type I interferon (IFN-I) shows complex roles in melanoma. Enhancing antitumor immunity requires balancing IFN-I signaling with interleukin-4 (IL-4) to overcome therapy resistance.

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Published on: March 24, 2015

Area of Science:

Immunology
Oncology
Molecular Biology

Background:

Metastatic melanoma presents significant therapeutic challenges, often linked to tumor microenvironment complexity.
Intratumoral type I interferon (IFN-I) has a dual role, potentially improving outcomes or promoting tumor growth.
Understanding the specific roles of IFN-I subtypes is crucial for effective cancer immunotherapy.

Purpose of the Study:

To investigate the paradoxical effects of different type I interferon (IFN-I) subtypes in a murine melanoma model.
To explore the interplay between IFN-I signaling and type 2 inflammation in controlling tumor growth.
To identify strategies for enhancing T cell-mediated antitumor immunity in nonresponsive solid tumors.

Main Methods:

Engineering murine B16 melanoma cells to overexpress various IFN-I subtypes.
Characterizing tumor immune phenotypes using RNA sequencing.
Restoring T cell-mediated rejection by introducing interleukin-4 (IL-4) via ectopic expression or adoptive T cell therapy.

Main Results:

Overexpression of certain IFN-I subtypes led to a spectrum of tumor outcomes.
Potent IFN-I signaling with diminished type 2 inflammation did not achieve durable tumor control.
Interleukin-4 (IL-4) introduction restored T cell-mediated tumor rejection in preclinical models.

Conclusions:

The IFN-I/IL-4 axis is critical for promoting effective antitumor immunity.
Targeting this axis could offer new therapeutic strategies for refractory solid tumors.
Stratification of patients based on this axis may improve immunotherapy response.