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Published on: December 24, 2015
PKC-θ function at the immunological synapse: prospects for therapeutic targeting
Alexandra Zanin-Zhorov1, Michael L Dustin, Bruce R Blazar
1Molecular Pathogenesis Program, Helen and Martin Kimmel Center for Biology and Medicine, Skirball Institute of Biomolecular Medicine, Department of Pathology, New York University School of Medicine, New York, NY 10016, USA.
Trends in Immunology
|July 8, 2011
Summary
Protein kinase C theta (PKC-θ) has a complex role in T cell function, impacting both effector and regulatory T cells. Targeting PKC-θ may offer therapeutic strategies for autoimmune and alloimmune diseases.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Protein kinase C theta (PKC-θ) is a key regulator of conventional effector T (Teff) cell function.
- The role of PKC-θ in T cells is complex, influencing Teff cell activation, survival, and immunological synapse (IS) stability.
- Recent studies indicate PKC-θ is crucial for regulatory T (Treg) cell development and function.
Purpose of the Study:
- To investigate the role of PKC-θ in the immunological synapse (IS).
- To examine the distinct localization of PKC-θ in Treg cells.
- To explore therapeutic implications of modulating PKC-θ in Teff and Treg cells for autoimmune and alloimmune diseases.
Main Methods:
- Analysis of PKC-θ localization within the IS.
- Investigation of PKC-θ's distinct functions in Treg cells.
- Evaluation of therapeutic potential of PKC-θ inhibition/modulation.
Main Results:
- PKC-θ negatively regulates the stability of the immunological synapse (IS).
- PKC-θ is essential for the development of natural CD4(+)Foxp3(+) regulatory T (Treg) cells.
- PKC-θ mediates negative regulation of Treg cell function.
Conclusions:
- PKC-θ plays a dual role in T cell immunity, affecting both effector and regulatory functions.
- Targeting PKC-θ in Teff cells can reduce effector function, while targeting it in Treg cells can enhance suppressor function.
- Modulating PKC-θ activity presents a potential therapeutic avenue for autoimmune and alloimmune conditions.

