- MD: Hacettepe University, Turkey
- D.Phil: University of Oxford, UK
- Postdoctoral Studies: NIH, member of the Laboratory of Immune System Biology, NIAID
Research Interests: Multiple Sclerosis (MS) and Neuroimmunology
Dr. Akkaya studies the mechanisms of regulatory T cell (Treg) mediated immune suppression in the context of autoimmunity and cancer using state-of-the-art techniques. Her lab is currently funded by the NIAID New Innovators Award (DP2) for exploring new precision therapies for autoimmune diseases and solid tumors.
Project 1: Deciphering the antigen mediated interactions and suppression mechanisms of human Tregs.
This project aims to implement a novel pipeline to reveal the specificities of dominant autoreactive effector T cell and Treg clones derived from type 1 diabetes mellitus and multiple sclerosis patients. The overarching goal of this study is to devise new antigen-targeted adoptive Treg therapies for autoimmune diseases.
Project 2: Discovering the molecular machinery underlying Treg interactions and Treg-mediated suppression.
This project aims to elucidate the signals provided to Tregs via antigen mediated contacts with dendritic cells. We compare Tregs and effector T cells using conventional techniques such as phosphoflow and western blot while also performing an unbiased analysis of phosphoproteome, to decipher the pathways underlying antigen- MHC Class II capture and antigen-specific suppression. Overall, this project will uncover the molecular basis of antigen-specific suppression performed by Tregs and identify key molecules that can potentially be targeted to fine-tune the Treg activity in autoimmunity and cancer.
Project 3: Determining the antigen-presentation capability of antigen-specific Tregs post- primary immune synapse.
In this project we focus on the events after Treg-APC synapse and investigate whether capturing antigen- MHC Class II (pMHCII) equips Tregs with the unique ability to target helper T cells during the physical absence of dendritic cells. We perform live confocal and intravital two-photon microscopy imaging as well as flow cytometry 1) to quantify direct contact between Tregs and helper T cells post-pMHCII acquisition 2) to determine modes of paracrine communication. Altogether, the findings from this project will describe how the Treg-T cell interactions shape peripheral tolerance and what mechanisms additional to pMHCII depletion are in place to prevent autoimmunity and also to promote tumor development.