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Biology subjects

Yates, A. E.

Publications and source records attributed to Yates, A. E..

2 recordsLinked to original sources

Computational discovery of precision therapeutics for hidradenitis suppurativa

Hidradenitis suppurativa (HS) is an underdiagnosed chronic, immune-mediated inflammatory skin disease that causes severe pain, drainage, and scarring, leading to significant physical and psychosocial burdens. HS is characterized by heterogenous molecular changes that are poorly understood, posing a significant challenge for drug development. Therapeutic options remain limited, and many patients experience disease relapse despite treatment. Therefore, precision medicine approaches are urgently needed to identify new therapies for HS. Here, we combine integrative transcriptomics, large-scale drug perturbational datasets, and translational immunology to identify sirolimus, pioglitazone, and fulvestrant as novel therapies for HS that can directly target and reverse the HS disease gene signature in immune cell types relevant to HS pathogenesis. Using a novel ex vivo HS skin model, sirolimus, pioglitazone, and fulvestrant inhibited T cell proliferation and activation, and suppressed the production of pro-inflammatory cytokines from HS skin. These results show that unbiased data-driven precision medicine approaches can identify novel therapies for HS and can serve more generally as a model approach for therapeutic discovery in other chronic inflammatory diseases. One Sentence SummaryData-driven precision medicine approach identifies sirolimus, pioglitazone, and fulvestrant as novel therapies for hidradenitis suppurativa

immunology↗

A Novel Whole Tissue Explant Model of Hidradenitis Suppurativa

Hidradenitis Suppurativa (HS) is a relatively common and highly morbid inflammatory skin disease. Due to our relatively limited understanding of HSs pathogenesis, there are currently insufficient treatment options available, and many patients medical needs are not being met. This is partly due to a scarcity of ex vivo human assays and animal models that accurately recapitulate the disease. To address this deficit, we have developed a whole-tissue explant model of HS to examine its pathogenic mechanisms and the efficacy of potential treatments within intact human tissue. We measured cytokine protein and RNA within whole tissue maintained in an agar-media solution, finding that IL-6 and IL-8 concentrations trended upwards in both HS explants and healthy controls, while IL-17A, IL-1{beta}, and TNF- exhibited increases in HS tissue alone. We also show that the explants were responsive to treatment with both dexamethasone and IL-2. Not only do our results show that this model effectively delivers treatments throughout the explants, but they also elucidate which cytokines are related to the explant process regardless of tissue state and which are related to HS tissue specifically, laying the groundwork for future implementations of this model.

immunology↗