Translational bioinformatics and data science for biomarker discovery in mental health: an analytical review.

Translational bioinformatics and data science play a crucial role in biomarker discovery as it enables translational research and helps to bridge the gap between the bench research and the bedside clinical applications. Thanks to newer and faster molecular profiling technologies and reducing costs, there are many opportunities for researchers to explore the molecular and physiological mechanisms of diseases. Biomarker discovery enables researchers to better characterize patients, enables early detection and intervention/prevention and predicts treatment responses. Due to increasing prevalence and rising treatment costs, mental health (MH) disorders have become an important venue for biomarker discovery with the goal of improved patient diagnostics, treatment and care. Exploration of underlying biological mechanisms is the key to the understanding of pathogenesis and pathophysiology of MH disorders. In an effort to better understand the underlying mechanisms of MH disorders, we reviewed the major accomplishments in the MH space from a bioinformatics and data science perspective, summarized existing knowledge derived from molecular and cellular data and described challenges and areas of opportunities in this space.

Suppressor T helper type 17 cell responses in intestinal transplant recipients with allograft rejection.

BACKGROUND: Intestinal transplant (ITx) rejection is associated with memory T helper type 17 cell (Th17) infiltration of grafted tissues. Modulation of Th17 effector cell response is facilitated by T regulatory (Treg) cells, but a phenotypic characterization of this process is lacking in the context of allograft rejection. METHODS: Flow cytometry was performed to examine the expression of surface receptors, cytokines, and transcription factors in Th17 and Treg cells in ITx control (n = 34) and rejection patients (n = 23). To elucidate key pathways guiding the rejection biology, we utilized RNA sequencing (RNAseq) and assessed epigenetic stability through pyrosequencing of the Treg-specific demethylated region (TSDR). RESULTS: We found that intestinal allograft rejection is characterized by Treg cellular infiltrates, which are polarized toward Th17-type chemokine receptor, ROR-γt transcription factor expression, and cytokine production. These Treg cell subsets have maintained epigenetic stability, as defined by FoxP3-TSDR methylation status, but displayed upregulation of functional Treg and purinergic signaling genes by RNAseq analysis such as CD39, in keeping with suppressor Th17 properties. CONCLUSION: We show that ITx rejection is associated with increased polarized cells that express a Th17-like phenotype concurrent with regulatory purinergic markers.