Interleukin-17D Promotes Pathogenicity During Infection by Suppressing CD8 T Cell Activity
Younghee Lee1, Jelita Clinton1, Chengfang Yao1
1Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Frontiers in Immunology
|June 28, 2019
Summary
Interleukin-17D (IL-17D) normally suppresses CD8 T cell activity. Removing IL-17D enhances immune protection against bacterial and viral infections by boosting T cell responses.
Area of Science:
- Immunology
- Infectious Diseases
Background:
- The IL-17 cytokine family plays roles in inflammation and host defense.
- The specific function of Interleukin-17D (IL-17D) in immunity is not well understood.
Purpose of the Study:
- To investigate the role of IL-17D in host defense against intracellular bacterial and viral infections.
- To elucidate the mechanism by which IL-17D influences immune cell activity during infection.
Main Methods:
- Comparative analysis of wild-type (WT) and IL-17D-deficient mice during Listeria and influenza A virus infections.
- Assessment of immune cell activity, particularly CD8 T cells and dendritic cells.
- Genetic manipulation including CD8 T cell depletion and RAG-deficient mouse models.
Main Results:
- IL-17D deficiency conferred protection against Listeria and reduced severity of influenza A virus infection.
- Loss of IL-17D led to enhanced CD8 T cell activity, crucial for controlling pathogen burden.
- IL-17D was found to suppress dendritic cell function, thereby regulating CD8 T cell responses.
- Non-hematopoietic IL-17D regulates protective immunity during infection.
Conclusions:
- Interleukin-17D (IL-17D) acts as a negative regulator of CD8 T cell immunity during intracellular bacterial and viral infections.
- IL-17D suppresses protective immune responses by inhibiting dendritic cell function.
- Targeting IL-17D may represent a novel therapeutic strategy to enhance host defense against specific pathogens.
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