Tzvia Abramson

Tzvia Abramson408-924-4872
DH 446


  • Post-doc: In Dr. David Relman lab - Department of Microbiology and Immunology Stanford University
  • Ph.D/B.S. - Mentored by Prof. Yossi Levy and Prof. Yoav Sharoni- Department of Medical Sciences, Ben Gurion University, Israel.

Courses Taught

  • BIO 141L - Laboratory of pathogenic microbiology
  • BIO 142L - Laboratory of pathogenic microbiology
  • MICRO 20 - Lecture and laboratory - General microbiology
  • BIO 233 - Immunology techniques
  • BIO 107 - Basic immunology- Lecture
  • BIO 107L - Basic immunology- labs
  • BIO 255 - Immunology Journal club

Research Interests

It is intriguing how despite common microbial recognition motives, some microbes are able to reside within our organs, evading detection by the immune system, others trigger a strong immune response that may harm both the microbe and the host and yet others, can be tolerated by the immune system such that they thrive in our body while causing chronic disease. The organs exposed to the external environment are lined with mucosal tissue and are constantly in direct contact with microbes. The mucosa comprise a specialized network of immune and residential cells that together sustain the mucosal immunity. Immune cells use specific pattern of cell surface molecules that guide their migration from the blood or lymph nodes to a target organ (trafficking/homing molecules). In my research lab, we are currently study several aspects of the involvement of trafficking molecules in prolonged infections and chronic diseases:

  1. Bordetella pertussis induces an acute, highly contagious respiratory disease in humans, which is manifested by high numbers of circulating immune cells. However, despite the immune response, the clearance of the pathogen and the resolution of the symptoms are prolonged rather similar to those of a chronic disease. In this project we speculate that bacterial components reduce the levels of surface trafficking molecules on immune cells, thereby inhibiting the homing of immune cells to the respiratory mucosa and clear the infection. The outcome of this project may implicate the content of the acellular vaccine currently used to immunize human against pertussis infections.
  2. Inflammatory bowel diseases (IBD) comprise several intestinal inflammatory conditions including Crohn’s Disease and Ulcerative Colitis that affect 50-100 per 100,000 of the population in California. Abnormalities of the immune system are especially implicated in these diseases. The immature form of antibody producing cells are called plasmablasts, and those that migrate to the gut express a cell surface trafficking molecule termed alpha4beta7. The goal of this project is to understand the effect of commonly used therapies in IBD on the level of plasmablasts and how these changes relate to the response to therapy can be used to monitor the pace of the diseased.
  3. A newly initiated project will explore the manipulation and up-regulation of trafficking molecules expressed on immunosuppressive mesenchymal stem cells and their ability to migrate to brain tissue and reduce the inflammatory and destructive responses in a mouse model of multiple sclerosis.

* Students with research interests in these fields are encouraged to contact me to further discuss specific projects available.


  1. Nguyen TM, Ravindra D, Kwong B, Waheed S, Ferguson R, Nicole Tarlton, Victoria Wu, Christopher S. Sequeira, Martina Bremer and Tzvia Abramson  (2012) Differential Expression of Alpha 4 Integrins on Effector Memory T Helper Cells during Bordetella Infections. Delayed Responses inBordetella pertussis. PLoS ONE 7(12):e52903. doi:10.1371/journal.pone.0052903
  2. Nicole J Tarlton, Caroline M Green, Nicole H Lazarus, Lusijah Rott, Anthony P Wong, Oren Abramson, Martina Bremer, Eugene C Butcher and Tzvia Abramson. Plasmablast Frequency and Trafficking Receptor Expression are Altered in Pediatric Ulcerative Colitis Inflamm Bowel Dis. 2012 Apr 5. doi: 10.1002/ibd.
  3. Abramson T, Kedem H, Relman DA 2008 Modulation of the NF-κB Pathway by Bordetella pertussis Filamentous Hemagglutinin. PLoS ONE3(11): e3825 doi: 10.1371/journal.pone.0003825
  4. Abramson T, Kedem H, Relman DA.” Differing modes of NF-kappaB activation by Bordetella pertussis filamentous hemagglutinin in macrophages” FOCIS2007 San Diego, CA.
  5. Abramson T, Kedem H, Relman DA.” Differing modes of NF-kappaB activation by Bordetella pertussis filamentous hemagglutinin in macrophages” ASM2002 Los Angeles CA.
  6. Abramson T., Kedem H. and Relman DA. Proinflammatory and proapoptotic activities associated with Bordetella pertussis Filamentous Hemagglutinin. Infection and Immunity, 69 (4) 2650-2658 (2001).
  7. Abramson T, Kedem H, Relman DA.” Bordetella pertussis (Bp) filamentous hemagglutinin (FHA) has proinflammatory pro-apoptotic activities” ASM2000.
  8. Abramson T, Kedem H, Relman DA. “Bordetella pertussis FHA (Bp-FHA) has a Direct Inflammatory and Cytotoxic Effect on the U-937 Monocytic Cell Line”. ICCAC1999.
  9. Sion-Vardi N., Kaneti J., Segal-Abramson T., Giat J., Levy J. and Sharoni Y. GnRH specific binding sites in normal and malignant renal tissue”. Journal of Urology 148(5):1568-70 (1992).
  10. Abramson-Segal T., Kitroser H., Levy J., Shally AV. and Sharoni Y. Direct effects of LHRH agonists and antagonists on MCF-7 mammary cancer cells. Proc. Natl.Acad. Sci.USA 15;89(6):2336-9. (1992).
  11. Abramson-Segal T., Levy J., Giat J. and Sharoni Y. Guanine nucleotide modulation of high affinity GnRH receptors in mammary tumors. Molec. Cell. Endocrinol. 85:109-106 (1992).
  12. Segal T., Levy J. and Sharoni Y. GnRH analogs stimulate Phospholipase-C activity in mammary tumor membranes: Modulation by GTP. Molec. Cell. Endocrinol. 53: 239-243 (1987).