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Type I and Type II Interferon Coordinately Regulate Suppressive Dendritic Cell Fate and Function during Viral
Cameron R Cunningham1, Ameya Champhekar1, Michael V Tullius2
1Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, United States of America.
Persistent infections trigger immunosuppressive programs. This study reveals how inflammation drives specific dendritic cells (DCs) to suppress T cell responses, offering new therapeutic targets for chronic viral infections.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Persistent viral infections induce chronic inflammation and potent immunosuppression, hindering T cell responses.
- Understanding the mechanisms that program immunosuppressive cell functions is crucial for controlling persistent infections.
Purpose of the Study:
- To elucidate the signals and mechanisms driving the development and function of immunosuppressive dendritic cells (DCs) during persistent viral infections.
- To investigate the roles of Interferon-gamma (IFNγ) and Type I Interferon (IFN-I) in programming DC immunosuppressive properties.
Main Methods:
- Utilized lymphocytic choriomeningitis virus (LCMV) infection model in mice.
- Investigated the differentiation of monocytes into immunosuppressive DCs induced by IFNγ.
- Examined the role of IFN-I in programming DC immunosuppressive functions and inhibiting conventional DCs.
- Analyzed signaling pathways including MyD88 and MAVS.
Main Results:
- IFNγ induces naive monocytes to differentiate into immunosuppressive DCs.
- IFN-I programs these DCs for potent T cell suppression and inhibits T cell-stimulating DCs.
- MyD88 signaling is essential for suppressive DC differentiation; MAVS signaling mediates inhibition of stimulatory DCs.
- Similar suppressive DC mechanisms were observed in Mycobacterium tuberculosis, HIV, and cancer models.
Conclusions:
- The induction and programming of immunosuppressive DCs during persistent infection are separable, pro-inflammatory driven mechanisms.
- Distinct pathogen recognition pathways bifurcate to promote different aspects of IFN-I-mediated immunosuppression.
- Targeting these underlying mechanisms could restore T cell function and control various persistent infections and diseases.
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