- Department of Veterans Affairs
Current research projects
My research has focused on cellular and molecular mechanisms in autoimmunity and intestinal fibrosis
- The role of cytokines responsible for inducing and/or mitigating intestinal inflammation and fibrosis
- The contribution of the gut microbiome to intestinal fibrosis using in vivo and in vitro models
Future research directions
- Evaluating the mechanisms responsible for induction of fibroblast-mediated fibrosis with direct and indirect microbial stimuli
- Determining novel cellular pathways involved in intestinal fibrosis and inflammation
In the news
Dr. Jacob graduated cum laude from the University of California, Berkeley where he studied philosophy and molecular biology. He then investigated immunologic mechanisms involving cytokines central to T cell, B cell and innate immune function in autoimmune diseases at the University of Southern California, prior to earning his medical degree from the Keck School of Medicine at USC. He completed specialty training in internal medicine at the Mount Sinai School of Medicine, New York and then joined UCLA as a gastroenterology fellow in 2014. He pursued additional research training at UCLA through the Specialty Training and Advanced Research (STAR) program where he received his PhD in molecular, cellular and integrative physiology. His doctoral work focused on the effects of tumor necrosis factor-like cytokine 1A and the microbiome on intestinal fibrosis in inflammatory bowel disease. He joined the Vatche and Tamar Manoukian Division of Digestive Diseases faculty at UCLA as an assistant professor-in-residence in 2018.
Farzaneh will be working as a research associate with Dr. Jacob, investigating cellular and molecular pathways involved in the gut microbiome's impact on intestinal fibrosis in Crohn's disease. She will examine the effects of specific bacterial species and microbial metabolites on fibroblast function in models of IBD. She will also evaluate how pro-fibrotic/inflammatory cytokines and the gut microbiome may work in concert to promote intestinal fibrosis.
Farzaneh has a master’s degree in medical microbiology, and holds a U.S. Patent for a medical biosensor kit. Her bachelor's degree is in cellular- molecular biology and microbiology. Before joining the department, Farzaneh worked with UCLA MIMG (Microbiology, Immunology and Molecular Genetics) department labs.
- Jacob N, Kumagai K, Abraham JP, Shimodaira Y, Ye Y, Targan SR, Michelsen KS, Shih DQ. Direct Signaling of TL1A-DR3 on Fibroblasts Induces Intestinal Fibrosis In Vivo. Manuscript in preparation
- Jacob N, Jacobs J, Kumagai K, Ha CWY, Kanazawa Y, Lagishetty V, Altmayer K, Hamill AM, Von Arx A, Balfour S, Devkota S, Braun J, Michelsen KS, Targan SR, Shih DQ. Differing Microbial Populations Induce Tl1a-mediated Intestinal Fibrosis. In Press, Mucosal Immunology, 2018
- Jacob N, Targan SR, Shih DQ. “Cytokine and Anti-Cytokine Agents as Future Therapeutics for Fibrostenosing IBD.” Fibrostenotic Inflammatory Bowel Disease, Ed. Florian Rieder, Springer International Publishing, 2018
- Jacob N, Targan SR, Shih DQ. Cytokine and anti-cytokine therapies in prevention or treatment of fibrosis in IBD. United European Gastroenterol J. 2016; 4:531-40
- Jacob N, Guo S, Mathian A, Koss MN, Gindea S, Putterman C, Jacob CO, Stohl W. B Cell and BAFF dependence of IFNa-exaggerated disease in systemic lupus erythematosus-prone NZM 2328 mice. The Journal of Immunology. 2011; 186: 4984-93
- Jacob N, Stohl W. Cytokine disturbances in systemic lupus erythematosus. Arthritis Research & Therapy. 2011; 13: 228
- Jacob N, Stohl W. Autoantibody-dependent and autoantibody-independent roles for B cells in systemic lupus erythematosus: past, present, and future. Autoimmunity. 2010; 43: 84-97
- Stohl W, Jacob N, Guo S, Morel L. Constitutive overexpression of BAFF in autoimmune-resistant mice drives only some aspects of systemic lupus erythematosus-like autoimmunity. Arthritis and Rheumatism. 2010; 62: 2432-42
- Jacob N, Yang H, Pricop L, Liu Y, Gao X, Zheng SG, Wang J, Gao HX, Putterman C, Koss MN,Stohl W, Jacob CO. Accelerated pathological and clinical nephritis in systemic lupus erythematosus-prone New Zealand Mixed 2328 mice doubly deficient in TNF receptor 1 and TNF receptor 2 via a Th17-associated pathway. The Journal of Immunology. 2009; 182: 2532-41