Protein kinase C theta is dispensable for suppression mediated by CD25+CD4+ regulatory T cells.
basic_science · Level V
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- Record sourced from PubMed, PMID 28531229.
- Also identified by DOI 10.1371/journal.pone.0175463 and PMC identifier 5439664.
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Abstract
The activation of conventional T cells upon T cell receptor stimulation critically depends on protein kinase C theta (PKCθ). However, its role in regulatory T (Treg) cell function has yet to be fully elucidated. Using siRNA or the potent and PKC family-selective pharmacological inhibitor AEB071, we could show that murine Treg-mediated suppression in vitro is independent of PKCθ function. Likewise, Treg cells of PKCθ-deficient mice were fully functional, showing a similar suppressive activity as wild-type CD25+CD4+ T cells in an in vitro suppression assay. Furthermore, in vitro-differentiated wild-type and PKCθ-deficient iTreg cells showed comparable Foxp3 expression as well as suppressive activity. However, we observed a reduced percentage of Foxp3+CD25+ CD4+ T cells in the lymphatic organs of PKCθ-deficient mice. Taken together, our results suggest that while PKCθ is involved in Treg cell differentiation in vivo, it is dispensable for Treg-mediated suppression.
Medical subject headings
- CD4 Antigens
- Forkhead Transcription Factors
- Interleukin-2 Receptor alpha Subunit
- Isoenzymes
- Protein Kinase C
- T-Lymphocytes, Regulatory