Human mesenchymal stromal cells (MSCs) rely on specific inflammatory disease microenvironments in order to carry out their anti-inflammatory actions in vivo. One of the barriers to the success of MSC therapy is the inability to identify potential responders. Macrophage migration inhibitory factor (MIF) has been identified to play a pivotal role in the pathogenesis of several inflammatory disorders including asthma. The aim of this thesis was to develop an understanding into the interaction between MIF and MSCs in a house dust mite (HDM) model of allergic asthma. Using humanised mice with either high- or low-expressing MIF promoter polymorphisms, we identified a dominant role of MIF allelic variants with the high expressing CATT7 mice exhibiting a more severe asthma phenotype. The CATT7 mice experienced significantly higher levels of eosinophilia, airway remodelling, and airway hyperresponsiveness. In vitro studies revealed the ability of high levels of hMIF to improve MSC migration, expansion and immunomodulation, thus, identifying MIF as a potential agent to enhance MSC therapeutic efficacy. High hMIF environments in vivo potentiated MSCs therapeutic effects with MSCs able to significantly attenuate airway inflammation and ameliorate airway remodelling in CATT7 mice compared to CATT5 or wildtype. Furthermore, we demonstrated that licensing MSCs with high levels of hMIF prior to administration can further enhance therapeutic efficacy through the upregulation of COX-2 expression. The data presented herein contributes to a broader understanding on how disease microenvironments can affect MSC therapeutic efficacy and identifies MIF as a potential biomarker for MSC success.