Aire expressing innate-like type 3 cells (Aire+ ILC3-like cells) are recently discovered subgroup of ILC3 cells. Conventional ILC3 cells are crucial in the response to extracellular pathogens due to their ability to rapidly produce and secrete cytokines. In contrast, Aire+ ILC3-like cells are equipped with powerful antigen presentation capacity and have striking ability to modulate the T-cell responses in antigen-specific manner. The ablation of Aire in ILC3 cells has a profound effect on T-cell responses during infection with opportunistic pathogen Candida albicans. However, the mechanism how Aire in ILC3 cells regulates T-cell stimulation and polarization remains largely elusive.
The proposed project is based on the genetic deletion of selected Aire-regulated effector molecules in ILC3 cells, followed by tracking of T-cell fate mainly during Candida albicans infection but also in the setting of other infectious and autoimmune diseases. Complex animal infectious or autoimmunity models, flow cytometry and single cell genomics will be used as the basic toolbox to dissect the outcome of genetic manipulation of Aire+ ILC3-like cells´ effector molecules during infection or autoimmunity. The proposed project is going to reveal important signals delivered by Aire+ ILC3-like cells to T-cells in order to modulate their polarization and regulation of effector T-cells fate. This is the essential prerequisite for design of intervention strategies during infection and for prediction of their outcomes.
The project is well suited for students with deep interest in immunology, biology of infectious diseases or host-pathogen interactions. Our team is deeply interested in host-pathogen interaction, antigen presentation by non-classical antigen presenting cells and regulation of adaptive immune responses. We are looking for talented, friendly and enthusiastic new lab member with proven laboratory experience. Although the strong background in immunology, cell biology and molecular biology is a great advantage, motivation is the most important requirement.Deadline is closed