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The effects of androgenetic alopecia development on immune function

About This PhD Project

Project Description

Androgen hormones can have significant effects on hair follicles in androgen sensitive regions of the scalp, beard, and other areas of skin. With the development of androgenetic alopecia (AGA) in both men and women, there is progressive miniaturization of androgen sensitive scalp hair follicles often associated with variable infiltration of affected skin by immune cells. The significance of the immune cell infiltration in AGA is poorly understood, and the effects of hair follicle miniaturization on immune privilege and immunostimulatory function in hair follicles is unknown.

Beyond the skin, development of AGA is also associated with increased risk of heart disease, diabetes and other pro-inflammatory conditions. Circumstantially, the apparent associations between AGA development and inflammatory cell activity suggest a functional interrelation. This project will investigate the potential for interaction between hormonal activity and inflammatory cell activity in AGA development.


1) Characterise the effects of androgen exposure on the expression of immune privilege related factors in androgen sensitive and androgen insensitive hair follicle tissues. This aim will involve culture of hair follicles and/or specific hair follicle mesenchyme cell types with dose concentrations of androgens. The cultured hair follicles/cells will be analysed for changes in immunostimulatory, chemoattractive, and immune privilege related factors using quantitative PCR, immunohistochemistry and/or western blotting.

2) Determine the functional changes in immunostimulation/immune privilege and inflammatory cell chemoattraction. This aim will involve conducting single culture and mixed lymphocyte assays using androgen exposed and non-androgen exposed hair follicle cells, and/or conditioned media, to define the degree of change in inflammatory cell activation response and cell migration ability.

3) Identify potential differences in cytokine/chemokine expression in blood samples from subjects with and without AGA. This aim will involve using ELISA assays and related analysis methods to determine the expression profiles of a select panel of inflammation related markers.

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