Gary Fathman


C. Garrison Fathman, MD, Professor of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine


Research Description: Dr. Fathman is a clinician scientist who has made seminal discoveries in diabetes and translational research. Among Dr. Fathman’s contributions to his field is the initial cloning of CD4 T lymphocytes in 1978. Dr. Fathman was one of the first to use monoclonal antibodies to treat animal models of autoimmunity. He was the first to use anti-CD4 antibodies to treat NOD disease, and to block allograft transplant rejection in diabetic NOD. He was among the first to use peptides of autoantigens to treat autoimmune disease models. A major recent finding in diabetes research was the identification of a splice form of a gene that regulated a non-thymic mechanism for inducing or maintaining peripheral tolerance in NOD that had similar isoform in human T1D that seemed to mimic the NOD gene function. He is currently using gene expression of peripheral blood cells in T1D patients and first-degree relatives to identify biomarkers of disease risk and progression.


Selected relevant publications (Stanford DRC Members in BOLD):

  1. Kodama K, Zhao Z, Toda K, Yip L, Fuhlbrigge R, Miao D, Fathman CG, Yamada S, Butte AJ, Yu L. Expression-Based Genome-Wide Association Study Links Vitamin D-Binding Protein With Autoantigenicity in Type 1 Diabetes. Diabetes 65(5):1341-9, 2016.
  2. Sosenko JM, Skyler JS, DiMeglio LA, Beam CA, Krischer JP, Greenbaum CJ, Boulware D, Rafkin LE, Matheson D, Herold KC, Mahon J, Palmer JP; Type 1 Diabetes TrialNet Study Group; Diabetes Prevention Trial-Type 1 Study Group (with CG Fathman). A new approach for diagnosing type 1 diabetes in autoantibody positive individuals based on prediction and natural history. Diabetes Care 38(2):271-6, 2015.
  3. Yip L, Fuhlbrigge R, Taylor C, Creusot RJ, Nishikawa-Matsumura T, Whiting CC, Schartner JM, Akter R, von Herrath M, Fathman CG. Inflammation and hyperglycemia mediate Deaf1 splicing in the pancreatic lymph nodes via distinct pathways during type 1 diabetes. Diabetes 64(2):604-17, 2015.
  4. Yip L, Taylor C, Whiting CC, Fathman CG. Diminished adenosine A1 receptor expression in pancreatic α-cells may contribute to the pathology of type 1 diabetes. Diabetes 62(12):4208-19, 2013.
  5. Yip L, Creusot RJ, Pager CT, Sarnow P, Fathman CG. Reduced DEAF1 function during type 1 diabetes inhibits translation in lymph node stromal cells by suppressing Eif4g3J. Mol Cell Biol. 13 (2):99-110, 2013.
  6. Junttila IS, Creusot RJ, Moraga I, Bates DL, Wong MT, Alonso MN, Suhoski MM, Lupardus P, Meier-Schellersheim M, Engleman EG, Utz PJ, Fathman CG, Paul WE, Garcia KC. Redirecting cell-type specific cytokine responses with engineered interleukin-4 superkines. Nat Chem Biol. 2012 Dec;8(12):990-8.
  7. Maecker HT, Lindstrom TM, Robinson WH, Utz PJ, Hale M, Boyd SD, Shen-Orr SS, Fathman CG. New tools for classification and monitoring of autoimmune diseases. Nat Rev Rheumatol. 2012 May 31;8(6):317-28.