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Diacylglycerol kinases in immune cell function and self-tolerance
Xiao-Ping Zhong1, Rishu Guo, Houde Zhou
1Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA. zhong001@mc.duke.edu
Immunological Reviews
|September 2, 2008
Summary
Diacylglycerol kinases (DGKs) regulate immune cell signaling. These enzymes control T-cell tolerance, mast cell activation, and cytokine production in macrophages and dendritic cells, impacting host defense.
Area of Science:
- Immunology
- Cell signaling
- Enzymology
Background:
- Diacylglycerol (DAG) and phosphatidic acid (PA) are crucial second messengers in immune cell signal transduction.
- Diacylglycerol kinases (DGKs) metabolize DAG to PA, influencing cellular responses.
- The specific roles of DGK isoforms in various immune cells are increasingly recognized.
Purpose of the Study:
- To elucidate the critical functions of diacylglycerol kinases (DGKs) in regulating diverse immune cell lineages.
- To investigate the dual roles of DGKs as both signal terminators and initiators in immune responses.
Main Methods:
- Analysis of DGK isoform function (alpha and zeta) in T cells, mast cells, dendritic cells, and macrophages.
- Investigating the impact of DGK activity on T-cell receptor and Toll-like receptor signaling pathways.
- Assessing the role of DGK products (PA) in immune cell activation and cytokine production.
Main Results:
- DGK alpha and zeta inhibit T-cell receptor signaling, promoting anergy and tolerance.
- DGKzeta differentially regulates mast cell activation, enhancing degranulation while reducing cytokine release.
- DGKzeta promotes pro-inflammatory cytokine production in dendritic cells and macrophages via PA, crucial for host defense against Toxoplasma gondii.
Conclusions:
- Diacylglycerol kinases (DGKs) are pivotal regulators of immune cell function across multiple lineages.
- DGKs act as both signal terminators (e.g., in T cells) and signal initiators (e.g., in macrophages/dendritic cells).
- Understanding DGK roles is essential for comprehending immune cell homeostasis and host defense mechanisms.
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