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The regulatory T cell and control of microvascular inflammation

The regulatory CD4+ T cell is an anti-inflammatory immune cell with a critical role in preventing inappropriate inflammation in the skin. This is demonstrated by the observation that patients with dysfunctional regulatory T cells are commonly affected by spontaneous skin inflammation. However, the mechanisms whereby regulatory T cells prevent skin inflammation are unknown. In order to control dermal inflammation, regulatory T cells must home to the skin from the bloodstream via interactions with endothelium lining the dermal microvasculature. Our laboratory has been investigating these interactions in a model of T cell-mediated skin inflammation, discovering that the nature of the interactions of regulatory T cells changes markedly at different phases of the skin inflammatory response. We hypothesise that these changes are important in the key step of resolution of skin inflammation. In this project we will investigate the cellular and molecular basis of these alterations in regulatory T cell and endothelial cell function in the inflamed skin. This project will use state of the art in vivo microscopy techniques, including spinning disk confocal & multi-photon microscopy, and regulatory T cell reporter (Foxp3-GFP) mice to enable direct visualization of regulatory T cell-endothelial cell interactions in vivo in the vasculature of the skin. It will involve intricate surgical procedures for preparation of the inflamed skin for microscopy procedures. This work will lead to an increased understanding of the molecular basis of the actions of regulatory T cells.
Essential criteria: 
Minimum entry requirements can be found here:
regulation of inflammation, regulatory T cell, imaging, intravital microscopy, skin, endothelial cells
School of Clinical Sciences at Monash Health / Hudson Institute of Medical Research » Medicine - Monash Medical Centre
Available options 
Time commitment 
Top-up scholarship funding available 
Physical location 
Monash Medical Centre Clayton

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