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Histone deacetylase 10 (HDAC 10) deacetylates Foxp3 and modulates its stability
10th Euro Global Summit and Expo on Vaccines & Vaccination
June 16-18, 2016 Rome, Italy

Suna Gu, Dahee Kim and Sang-Myeong Lee

Chonbuk National University, Republic of Korea

Posters & Accepted Abstracts: J Vaccines Vaccin

Abstract:

Regulatory T cells (Tregs) have been shown to play a crucial role in maintaining self-tolerance and suppressing autoimmunity. The Forkhead family transcription factor Foxp3 is a key molecule necessary and sufficient for Tregs development and function. However, the molecular mechanisms by which Foxp3 regulate phenotypic (anergic) and functional (suppressive) characteristics of Tregs are not completely understood yet. Several studies have shown that Foxp3 regulates Tregs function by interfering with the transcription activities of various transcription factors including NFAT, NF-kB and AP-1. Previous studies have demonstrated that histone deacetylase (HDAC)-9 deacetylase Foxp3 to suppress Foxp3 activity and deacetylase inhibitor (HDACi) increases Foxp3 gene expression and suppressive function of Tregs. Previous studies have suggested that HDAC-1, 6 and 7 also interact with FoxP3. In the present study, we have identified HDAC-10 as another HDAC which interacts with Foxp3 via yeast-two hybrid assay. We confirmed the interaction between HDAC10 and Foxp3 in HEK293 cells by co-immunoprecipitation. This interaction was required the dimerization of Foxp3. In addition, Foxp3 and HDAC-10 were co-localized in the nucleus of Tregs. Interestingly, we found that HDAC10 deacetylated Foxp3 and inhibited the ubiqutination of Foxp3, which increase the stability of Foxp3. These findings suggest that HDAC-10 is a new FoxP3 interaction partner in Tregs which is possibly involved in the function of FoxP3 in these cells.

Biography :

Suna Gu is currently a PhD student under Professor Sangmyeong Lee at Chonbuk National University, Republic of Korea. Her current area of research is protein-protein interactions in T regulatory cells (Tregs). She has authored one paper on effect of polymorphisims in the GBP1, MX1 and CD163 genes on host responses to PRRSV infection in pigs in Journal of Veterinary Microbiology.

Email: gsnsuda2007@126.com