The PI3K p110δ regulates expression of CD38 on regulatory T cells

Daniel T. Patton, Marcus D. Wilson, Wendy C. Rowan, Dalya R. Soond, Klaus Okkenhaug*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


The PI3K pathway has emerged as a key regulator of regulatory T cell (Treg) development and homeostasis and is required for full Treg-mediated suppression. To identify new genes involved in PI3K-dependent suppression, we compared the transcriptome of WT and p110δD910A Tregs. Among the genes that were differentially expressed was the gene for the transmembrane cyclic ADP ribose hydrolase CD38. Here we show that CD38 is expressed mainly by a subset of Foxp3+CD25+CD4+ T cells originating in the thymus and on Tregs in the spleen. CD38high WT Tregs showed superior suppressive activity to CD38low Tregs, which failed to upregulate CD73, a surface protein which is important for suppression. However, Tregs from heterozygous CD38+/- mice were unimpaired despite lower levels of CD38 expression. Therefore, CD38 can be used as a marker for Tregs with high suppressive activity and the impaired Treg function in p110δD910A mice can in part be explained by the failure of CD38high cells to develop.

Original languageEnglish
Article numbere17359
JournalPLoS ONE
Issue number3
Publication statusPublished - 10 Mar 2011


Dive into the research topics of 'The PI3K p110δ regulates expression of CD38 on regulatory T cells'. Together they form a unique fingerprint.

Cite this