Patricia A. Pioli, PhD
Assistant Professor of Microbiology and Immunology
Microbiology and Immunology
Dartmouth Medical School, Ph.D. 2001
George Washington University, B.S. 1993
Molecular and Cellular Biology Graduate Programs
Program in Experimental and Molecular Medicine
Dartmouth Medical School
Lebanon NH 03756
Office: 644E Borwell Building
autoimmunity, cancer immunotherapy, molecular immunology, endocrinology
Rotations and Thesis Projects:
1. Determine how aberrant regulation of miRNAs affects activation of macrophages in autoimmune systemic sclerosis (scleroderma)
2. Identify the role that macrophages play in the immune/fibrotic axis in scleroderma
3. Determine how modulation of the tumor immune landscape (microenvironment) can be used to combat cancer
Dr. Pioli received a B.S. in biology from George Washington University in 1993 and a Ph.D. in biochemistry from Dartmouth Medical School in 2001. She performed post-doctoral research with Dr. Paul Guyre at Dartmouth from 2001-2004, studying the mechanisms by which cortisol influences macrophage activation and immune function. She was appointed Research Assistant Professor of Physiology from 2004-2010. In July 2010, Dr. Pioli joined the faculty of Dartmouth Medical School as Assistant Professor in the Department of Obstetrics and Gynecology and Microbiology and Immunology.
Systemic Sclerosis Dermal Fibroblasts Induce Cutaneous Fibrosis Through LOXL4: New Evidence from 3D Skin-like Tissues.
Macrophages in Systemic Sclerosis: Novel Insights and Therapeutic Implications.
Microbiome dysbiosis is associated with disease duration and increased inflammatory gene expression in systemic sclerosis skin.
The Stress Hormone Cortisol Enhances Interferon-υ-Mediated Proinflammatory Responses of Human Immune Cells.
Mycophenolate Mofetil Treatment of Systemic Sclerosis Reduces Myeloid Cell Numbers and Attenuates the Inflammatory Gene Signature in Skin.
A novel multi-network approach reveals tissue-specific cellular modulators of fibrosis in systemic sclerosis.
Bromodomain inhibitors, JQ1 and I-BET 762, as potential therapies for pancreatic cancer.
The triterpenoid CDDO-imidazolide reduces immune cell infiltration and cytokine secretion in the KrasG12D;Pdx1-Cre (KC) mouse model of pancreatic cancer.
CDDO-Me Redirects Activation of Breast Tumor Associated Macrophages.
Glucocorticoids enhance the in vivo migratory response of human monocytes.