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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
p204-Mediated innate antiviral responses in mouse adipose cells and their effects on cell functions
Lili Yu1, Peng Liu2, Zhenghui Liu2
11] Department of Cell Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China [2] Department of Immunology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Abstract:
Viruses can infect adipose tissues. However, innate antiviral responses in adipose cells and their effects on adipocyte function have not yet been intensively investigated. In this study, p204-initiated innate antiviral responses in mouse adipose cells were examined. Cytosolic DNA sensor p204 and its signaling adaptor stimulator of interferon (IFN) genes (STING) were constitutively expressed in primary preadipocytes. Synthetic herpes simplex viral DNA (HSV60), a p204 ligand, induced type I IFN expression by activating IFN regulatory factor 3. Major antiviral proteins, including IFN-stimulating gene 15, 2',5'-oligoadenylate synthetase and Mx GTPase 1, in preadipocytes were upregulated by HSV60. HSV60-triggered innate antiviral responses were significantly reduced by inhibition of p204 signaling with specific small interfering RNA targeting p204 or STING. HSV60 inhibited the differentiation of preadipocytes to mature adipocytes and enhanced the proliferation of adipose cells. Moreover, HSV60 induced innate antiviral responses in mature adipocytes and inhibited expressions of several adipokines, including leptin, adiponectin and resistin. These results indicated that p204 initiated innate antiviral responses in adipose cells, thereby modulating adipocyte function.
Insights
Viruses trigger innate antiviral responses in mouse adipose cells via the p204-STING pathway. This response impacts adipocyte differentiation, proliferation, and adipokine production, revealing a novel role for adipose tissue in antiviral defense.
Area of Science:
- Immunology
- Cell Biology
- Endocrinology
Background:
- Adipose tissues are susceptible to viral infections.
- Innate antiviral responses in adipocytes and their functional impact remain underexplored.
Purpose of the Study:
- To investigate p204-initiated innate antiviral responses in mouse adipose cells.
- To determine the effects of these responses on adipocyte function and differentiation.
Main Methods:
- Primary mouse preadipocytes and mature adipocytes were used.
- Synthetic herpes simplex viral DNA (HSV60) was employed as a p204 ligand.
- p204 and STING signaling pathways were analyzed using siRNA inhibition.
Main Results:
- HSV60 induced type I interferon expression and upregulated antiviral proteins in preadipocytes via p204-STING signaling.
- HSV60 inhibited preadipocyte differentiation, enhanced adipose cell proliferation, and modulated adipokine expression in mature adipocytes.
- Inhibition of p204 or STING signaling reduced HSV60-induced antiviral responses.
Conclusions:
- p204 initiates innate antiviral responses in adipose cells.
- These responses modulate adipocyte differentiation, proliferation, and function, including adipokine production.
- Adipose tissue plays a role in innate antiviral immunity.
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