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CD39 and control of cellular immune responses
Karen M Dwyer1, Silvia Deaglio, Wenda Gao
1Immunology Research Centre, St. Vincent’s Health, Melbourne, Australia.
Purinergic Signalling
|April 12, 2008
Summary
CD39, an ecto-enzyme, regulates immune responses by modulating extracellular nucleotides and adenosine. It distinguishes T regulatory cells and is crucial for immune suppression, offering therapeutic potential for autoimmune diseases.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- CD39 is an ecto-enzyme crucial for extracellular nucleotide metabolism.
- Its role in immune responses, particularly T cell regulation, is not fully understood.
- CD39, along with CD73, generates adenosine, impacting P2 and adenosine receptor signaling.
Purpose of the Study:
- To investigate the expression and function of CD39 in T cell subsets.
- To elucidate the role of CD39 in T regulatory cell (Treg) function and immune suppression.
- To explore the therapeutic potential of targeting CD39 in immune-mediated diseases.
Main Methods:
- Analysis of CD39 expression in quiescent and activated T cell subsets.
- Functional studies on CD39's role in Treg-mediated suppression.
- Investigation of purinergic signaling pathways involving CD39, CD73, and adenosine receptors.
- Phenotypic analysis of Cd39-null mice to assess in vivo immune responses.
Main Results:
- CD39, with CD73, effectively distinguishes T regulatory cells (Tregs) from other T cells in mice and humans.
- CD39 is integral to Treg suppressive function, partly via adenosine modulation.
- Coordinated CD39/CD73 and A2A receptor signaling creates an immunoinhibitory loop affecting Th1/Th2 responses.
- Cd39-null mice exhibit spontaneous autoimmune disease features linked to Th1 immune deviation.
Conclusions:
- CD39 plays a critical role in regulating immune responses through purinergic signaling.
- CD39 is a key component of Treg suppressive machinery and distinguishes Tregs.
- Targeting CD39 and purinergic signaling offers potential therapeutic strategies for immune-mediated diseases.
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