Rationale: Alterations in the resolution of the immune response can lead to chronic inflammation, driving diseases such rheumatoid arthritis, atherosclerosis or obesity. Additionally, blocking the resolution phase can potentiate the immune response, desirable in settings such as cancer. Hence, regulating the resolution of the immune response can be of benefit in many different disease settings. However, the molecular machinery that underpins this process is not well understood. Our laboratories have discovered signals that drive immunoresolution in human T cells, specifically how the potent anti-inflammatory cytokine IL-10 is regulated by external signals that control the expression of the transcription factor c-Maf. Moreover, we have also identified of a unique role of cellular metabolism in this process.
Aims: This project aims to uncover the molecular drivers of c-Maf expression, as well as the discovery of new candidate pathways that drive immunoresolution in human T cells. Once identified, pathways and molecules will be interrogated in different disease settings by analysing human samples from patients with chronic inflammatory diseases, metabolic disorders or cancer.
Techniques: This project will involve both dry and wet laboratory skills. Our laboratories have generated several -omics datasets (RNAseq, scRNAseq) that will be analysed by the student, together with publicly available ones, using R programming. Wet lab skills include general cellular and molecular immunoassays such as flow cytometry, proliferation, immune cell isolation and culture and quantitative PCR. Specific immunometabolic assays and imaging techniques (i.e. Imagestream) will also be part of this project.
Objectives:
Year 1: molecular dissection of immunoresolution pathways in health. Interrogation of -omics datasets to discover new intersections between metabolism and immune signatures. In vitro validation of these pathways.
Year 2-3: follow up on the new signatures. Genetic manipulation in cell lines or primary cells.
Year 2-3: interrogate the relevant pathways in disease models by accessing our human samples biobank.