JAZ2 is important for Treg function

JAZF1 mRNA expression in Treg lentivirally-transduced to knockdown FOXP3

JAZF1 mRNA expression in Treg lentivirally-transduced to knockdown FOXP3

Study novel targets for autoimmune therapy via the validation of Foxp3 regulated genes critical for treg function.

Regulatory T cells (Treg) are crucial for a balanced, responsive immune system. They are crucial for maintaining tolerance, and autoimmune disease is linked to the loss of function of Treg. FOXP3 is a master transcription factor essential for the formation and function of Treg, and it shapes their function by enforcing a suppressor phenotype.

MicroRNAs can finely control the expression of many genes and are crucial for the development and function of Treg. We have shown that miRs can form feed forward loops with FOXP3 to prevent expression of genes in Treg. JAZ1 is a transcription factor with a very well established role in development.

However, we have identified JAZ1 as being up regulated by FOXP3 where it may have a role in maintaining the suppressive function of Treg. Interestingly it is also target of miR31, which is itself a putative target of FOXP3 in Treg. Thus JAZ1 expression expression is tightly regulated by FOXP3 in Treg.

In contrast, JAZ1 is down-regulated in Thelper cells, which express high levels of miR31. Thus, JAZ1 may have a unique function in the CD4+ immune compartment and characterising the role and regulation of JAZ1 in Treg will provide crucial information for comparative analysis with Treg from autoimmune disease patients.

Professor Simon Barry


Professor Simon Barry

Co-supervisor: Dr Cheryl Brown

Research area: Molecular immunology

Recommended honours enrolment: Honours in Molecular and Biomedical Science

Tagged in Honours projects - Molecular and biomedical science, Honours projects - Simon Barry, Honours projects - Cheryl Brown, Honours projects - Molecular and biomedical science: Microbiology and immunology