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Julie Jameson, PhD

Assistant Professor Adjunct
Department of Immunology and Microbiology
California Campus
Scripps VIVO Scientific Profile
(858) 784-8157

Research Focus

Function of γδ T Cells in Infection and Tissue Repair γδ T cells become activated by infected or damaged cells to produce cytokines and growth factors. Understanding how these unique T cells function and their requirements for activation is important for diseases such as obesity and type 2 diabetes in which these cells have become dysfunctional. We have previously shown that skin γδ T cell-derived growth factors play roles in skin homeostasis and wound repair. We have also determined that skin γδ T cells are dysregulated in non-healing wounds during obesity and type 2 diabetes. Cross-talk between key growth factors produced by skin γδ T cells and their receptors expressed on keratinocytes are being examined. In other studies we are investigating the function of skin γδ T cells during rapamycin treatment. Rapamycin (sirolimus, Rapamune) is approved by the U.S. Food and Drug Administration for prophylaxis of acute rejection. However patients that receive rapamycin report an increased incidence of wound healing complications. We are currently examining mechanisms relating to the mTOR pathway that may contribute to this skin γδ T cell dysfunction. Last we are examining how γδ T cells respond and control influenza infection. We have shown that influenza-infected cells activate γδ T cells to produce antiviral cytokines. We are currently investigating the mechanism of this activation. Once we fully understand how γδ T cells T cells become activated, it may be possible to design therapies that enhance the ability of these immune cells to suppress infection or heal diabetic ulcers and other chronic wounds.


B.A., Biology, University of California, Santa Barbara, 1994
Ph.D., Immunology and Virology, University of Massachusetts Medical Center (UMass Worcester), 1999

Professional Experience

1994-1999          Ph.D. Immunology and Virology with Dr. Francis Ennis, University of Massachusetts Medical Center, Worcester, MA    

1999-2004          Research Associate with Dr. Wendy Havran, The Scripps Research Institute, La Jolla, California

2004-2005          Senior Research Associate, The Scripps Research Institute, La Jolla, California

2005-present       Assistant Professor, The Scripps Research Institute, La Jolla, California

Awards & Professional Activities

Organizing committee and session chair, International γδ T Cell Conference (2006) Leukemia and Lymphoma Society Special Fellow (2003-2006), San Diego Cutaneous Biologists (2006-present), Director TSRI Summer Immunology Internship Program (2007-present)

Selected References

All Publications

Terajima, M., Cruz, J., Leporati, A.M., Orphin, L., Babon, J.A., Co, M.D., Pazoles, P., Jameson, J., and Ennis, F.A. (2008). Influenza A virus matrix protein 1-specific human CD8+ T-cell response induced in trivalent inactivated vaccine recipients. J. Virol. 82:9283.

Mills, R.E., Taylor, K.R., Podshivalova, K., McKay, D.E., and Jameson, J.M. (2008). Defects in skin γδ T cell function contribute to delayed wound repair in rapamycin-treated mice. J. Immunol. 181:3974.

Mills, R.E. and Jameson, J.M. (2009). T cell dependence on mTOR signaling. Cell Cycle. 15:545.

Toulon, A., Breton, L., Tenenhaus, M., Bhavsar, D., Lanigan, C., Rudolph, R., Jameson, J., and Havran, W. (2009). A role for human skin resident T cells in wound healing. J. Exp. Med. 206:743-750.

Taylor, K., Mills, R., Costanzo, A., and Jameson, J. (2010). gd T cells are reduced and rendered unresponsive by hyperglycemia and chronic TNF-a in mouse models of obesity and metabolic disease. PLoS One. 5:e11422. PMCID: 2896399.

Jameson, J.M., Cruz, J., Costanzo, A., Terajima, M., and Ennis, F.A. (2010). A role for the mevalonate pathway in the induction of subtype cross-reactive immunity to influenza A virus by human gd T lymphocytes. Cell. Immunol. 264:71. PMCID: 2905741.


A Skin Cell Revisited

Mysterious γδ T Cells Promoting Wound Repair