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Functional Characterization of Regulatory Macrophages That Inhibit Graft-reactive Immunity
Published on: June 7, 2017
Inhibition of tumor rejection by gammadelta T cells and IL-10
Yong Ke1, Linda M Kapp, Judith A Kapp
1Departments of Ophthalmology, Pathology and the Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA.
Abstract:
Although many tumors express tumor-specific antigens, most fail to stimulate effective immune responses. Tumors generally lack co-stimulatory molecules, which can lead to tolerance of tumor-specific T cells and progressive tumor growth. Here, we demonstrate that the ovalbumin (OVA) transfected EL4 tumor, E.G7-OVA, grows progressively in syngeneic mice even though the tumor can be rejected if the mice are immunized with OVA in adjuvant. E.G7-OVA grew more rapidly in RAG-1 deficient than sufficient mice suggesting that normal mice make an abortive immune response to this tumor. Depletion of gammadelta T cells or IL-10 augmented the ability of B6 mice to reject E.G7-OVA. Spleen cells from normal, but not IL-10 knockout, mice reconstituted rapid tumor growth in gammadelta T cell-deficient mice. Thus, gammadelta T cells play an important role in preventing immune elimination of this tumor by a mechanism that directly or indirectly involves IL-10.
Insights
Tumors often evade immune detection. This study reveals that gammadelta T cells, through Interleukin-10 (IL-10), suppress anti-tumor immunity, promoting tumor growth.
Area of Science:
- Immunology
- Cancer Research
- Tumor Microenvironment
Background:
- Tumors frequently express tumor-specific antigens but fail to elicit effective anti-tumor immune responses.
- Lack of co-stimulatory molecules in tumors can induce tolerance to tumor-specific T cells, leading to tumor progression.
- The E.G7-OVA (EL4 tumor transfected with ovalbumin) model in mice demonstrates progressive tumor growth despite antigen expression.
Purpose of the Study:
- To investigate the role of specific immune cell populations and cytokines in the immune evasion of the E.G7-OVA tumor.
- To elucidate the mechanisms by which tumors escape immune surveillance and promote their own growth.
- To identify potential targets for enhancing anti-tumor immunity.
Main Methods:
- Utilized syngeneic mouse models, including RAG-1 deficient and sufficient mice, to assess tumor growth dynamics.
- Employed experimental depletion of gammadelta T cells and utilized Interleukin-10 (IL-10) knockout mice.
- Assessed tumor rejection and growth kinetics following immunization with ovalbumin (OVA) in adjuvant.
- Transferred spleen cells from normal and IL-10 knockout mice into gammadelta T cell-deficient recipients.
Main Results:
- E.G7-OVA tumors grew progressively in syngeneic mice, indicating an abortive immune response in normal mice.
- Depletion of gammadelta T cells or IL-10 significantly enhanced the rejection of E.G7-OVA tumors in B6 mice.
- Spleen cells from normal mice reconstituted rapid tumor growth in gammadelta T cell-deficient mice, while cells from IL-10 knockout mice did not.
Conclusions:
- Gammadelta T cells play a critical role in preventing the immune elimination of the E.G7-OVA tumor.
- The mechanism by which gammadelta T cells inhibit anti-tumor immunity involves, directly or indirectly, the cytokine IL-10.
- Targeting gammadelta T cells or modulating IL-10 may represent a viable strategy to overcome tumor-induced immune tolerance and promote tumor rejection.
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