About Dr. Maria Serena Longhi
Maria Serena Longhi, MD, PhD
Associate Professor of Anaesthesia, Harvard Medical
Deputy Director of the Center of Inflammation Research, Department of Anesthesia, Critical Care and Pain Medicine, BIDMC
Dr. Maria Serena Longhi's research aims at defining how immune responses are regulated in chronic inflammatory statuses and in autoimmune disorders, including inflammatory bowel disease and autoimmune hepatitis. Her research program includes the following areas of interest:
Interactions between purinergic, hydrocarbon and oxygen mediated pathways in inflammatory bowel disease. Dr. Longhi's laboratory has found that effector Th17 cells obtained from the peripheral blood and lamina propria of Crohn's disease patients express low levels of CD39, an ectonucleotidase that is key to immune homeostasis by hydrolyzing pro-inflammatory nucleotides into immunosuppressive adenosine. Defective CD39 expression derives from impaired response of Th17 cells to ligands of aryl hydrocarbon receptor (AhR), a receptor for toxins/xenobiotics that also modulates adaptive immunity. Recent studies from her laboratory have shown that in Crohn's disease poor response to AhR ligands results from low oxygen levels, derived from protracted tissue inflammation. Her current research in this area aims at defining how alterations in the CD39, AhR and oxygen pathways can be therapeutically corrected.
Regulation of AhR signaling in autoimmune hepatitis. Dr. Longhi aims to identify key mechanisms that lead to functional impairment of regulatory T cells (Treg), a lymphocyte subset central to immunotolerance maintenance. Multiple mechanisms contribute to Treg impairment in patients with autoimmune hepatitis. As part of these investigations Dr. Longhi's laboratory is currently defining the alterations in AhR signaling pathways leading to Treg dysfunction in this autoimmune condition.
Post-transcriptional regulation of CD39 in inflammatory bowel disease. Dr. Longhi is defining the role of endogenous antisense RNAs, as modulators of CD39 expression and activity in both regulatory and effector cells in inflammatory bowel disease. Factors contributing to antisense RNA upregulation in Tregs and Th17 cells are also investigated.
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