Mucosal-associated invariant T (MAIT) cells are subset of innate-like unconventional T cells, characterised by the expression of a non-MHC restricted, semi-invariant T cell receptor (TCR); with a significant role in modulating host-protective responses to bacterial and viral pathogens. Upon activation, MAIT cells upregulate a potent effector programme, associated with robust proliferation, and the expression of a milieu of cytokines and cytolytic molecules. Such effector reprogramming is underpinned by proteome remodelling, rapid de novo biosynthesis, and increased metabolic flux. Therefore, MAIT cells are reliant on enhanced nutrient uptake to support their capacity to respond appropriately to challenge; and thus, nutrient availability is considered a limiting factor for MAIT cell activation. This is an important consideration to uphold in the context of disease settings such as infection, cancer, and obesity, where environmental nutrient availability can become perturbed. Gaining a complete understanding of the metabolic and nutrient underpinnings of MAIT cell effector responses is thus pertinent to our understanding of how these can responses become dysfunctional in disease. In this thesis, we aim to elucidate further our current understanding of MAIT cell metabolism, and the nutritional requirements underpinning the effector programme. Specifically, we highlight a novel role for iron uptake in dictating MAIT cell metabolic fitness downstream of TCR triggering, and characterise significant dysfunction under iron-deplete conditions. In addition, we describe for the first time, the metabolic responses of human MAIT cells to innate cytokine stimulation, and characterise a significant divergence from the TCR driven phenotype. Finally, we elucidate the importance of a functioning glutamine-MYC axis in supporting both metabolic rewiring and effector reprogramming in activated human MAIT cells. Overall, this PhD thesis contributes novel insights into MAIT cell metabolism in the context of both TCR-dependent and TCR-independent signalling pathways; and further demonstrates how environmental nutrient availability can shape host immune responses.