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Immune Cell Biology

The goal of the immune cell biology research group, led by Professor Franca Ronchese, is to gain a better understanding of the initiation of allergic, or “T helper 2” (Th2), immune responses. These immune responses are associated with a characteristic inflammation profile that includes cells such as eosinophils, basophils, and mast cells, antibodies such as IgE, and cytokines such as IL-4, IL-5 and IL-13. While the effector phase of the Th2 response is well characterised, its early phases are not nearly as well understood. A number of Th2-inducing factors have been discovered, but none of these appears to play an essential role across different allergens and immune responses, suggesting that key factors that drive the differentiation of Th2 cells may still be unidentified.

Our current studies focus on dendritic cells, a rare type of immune cells whose function is to initiate immune responses. Dendritic cells are found in most tissues in our bodies and especially in the skin, the intestinal tract, and the airway. We have perfected techniques to label allergens with fluorescent markers, monitor their uptake by dendritic cells in vivo, and follow their transport to lymph nodes where they initiate immune responses. By using these fluorescence-labelled antigens in combination with flow cytometry and transcriptomics, we are able to characterise in detail how allergen uptake alters the properties of dendritic cells and endows them with the ability to initiate Th2 immune responses. Results from these studies show that allergens impact the immune system at several levels, acting on dendritic cells directly, and also indirectly via the induction of innate cytokines in the tissue environment. By carrying out functional experiments we can alter or block the signalling of these innate cytokines in dendritic cells, assess their contribution to dendritic cell development, their expression of key mediators, and their priming of Th2 immune responses and subsequent allergic inflammation.

To increase the specificity of our models, we are also comparing allergen-treated dendritic cells to dendritic cells that have been exposed to other micro-organisms, such as bacteria and fungi, that prime Th responses of different phenotypes such as Th1 or Th17. We plan to compare the transcriptomes of dendritic cells exposed to these various stimuli to those of dendritic cells exposed to allergens. We expect that these studies will enable us to define the dendritic cell “Th2 signature” with a high level of precision.