James D. Gorham, MD, PhD
Adjunct Professor of Pathology
Adjunct Professor of Microbiology and Immunology
Microbiology and Immunology
New York University School of Medicine, MD 1992
New York University, PHD 1991
New York University, MS 1989
Haverford College, BA 1984
Dr. Gorham received his B.A. in Biology from Haverford College in 1984, his Ph.D. in Biochemistry from New York University in 1991 and his M.D. from New York University in 1992. He did postdoctoral training at Washington University, where he also completed a residency in Clinical Pathology and was Chief Resident (1997 - 1998). In 1998, he joined Dartmouth Medical School as Assistant Professor in the Department of Pathology with a secondary appointment in the Department of Microbiology and Immunology. He completed a Clinical Fellowship in Transfusion Medicine in 2009 at DHMC. He was promoted to Associate Professor in 2004 and to Professor in 2010.
Molecular and Cellular Biology Graduate Programs
Norris Cotton Cancer Center
The Geisel School of Medicine at Dartmouth
Department of Pathology, HB 7600
1 Medical Center Drive
Lebanon NH 03756
Asst. Phone: 603-650-8266
Genetic regulation of red blood cell storage
Liver Tolerance and Autoimmunity
The microbiota and regulation of liver injury
Organizer and lecturer of Autoimmunity block, DMS MCB Graduate Course 146 (Immunotherapy)
Geisel Year 1 - General Pathology
Rapid ADAMTS13 availability impacts treatment for microangiopathic hemolytic anemia and thrombocytopenia.
Cirrhosis and dysbiosis: New insights from next-generation sequencing.
Coincidental loss of DOCK8 function in NLRP10-deficient and C3H/HeJ mice results in defective dendritic cell migration.
Appropriate development of the liver Treg compartment is modulated by the microbiota and requires TGF-β and MyD88.
The microbiota regulates susceptibility to Fas-mediated acute hepatic injury.
1 + 1 = 3: Development and validation of a SNP-based algorithm to identify genetic contributions from three distinct inbred mouse strains.
Liver inflammation in a mouse model of Th1 hepatitis despite the absence of invariant NKT cells or the Th1 chemokine receptors CXCR3 and CCR5.
MDSC in autoimmunity.
Type 1 T helper cells induce the accumulation of myeloid-derived suppressor cells in the inflamed Tgfb1 knockout mouse liver.
The role of Ifng in alterations in liver gene expression in a mouse model of fulminant autoimmune hepatitis.