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Tonya J. Webb, PhD

Academic Title:

Associate Professor

Primary Appointment:

Microbiology and Immunology

Administrative Title:

Assistant Director for Diversity, Equity and Inclusion


HSF-I, 380

Phone (Primary):




Education and Training

Prairie View A&M University, BS, Biology, 1998

Indiana University, PhD,Microbiology and Immunology, 2003

Indiana University School of Medicine, Postdoctoral fellow, Immunology, 2005

Johns Hopkins, Postdoctoral fellow, Cancer Immunology, 2009


Dr. Webb is a leading immunologist and research scientist who is recognized for her studies focused on the modulation of CD1d-mediated NKT cell activation for cancer immunotherapy using natural and artificial platforms.

NKT cells recognize lipid antigen presented in the context of CD1d molecules. Following activation, NKT cells rapidly secrete both Th1 and Th2 cytokines and can mediate cytolytic activity. Therefore, NKT cells can both directly, through cytotoxicity, and indirectly, through activation of other effector cells, mediate anti-tumor immunity. Consequently, NKT cells constitute an important subset of T cells that can play an important role in regulating the host's anti-tumor immune response. However, cancer patients have a reduction in both NKT cell number and function, and these deficits currently limit the potential clinical application of NKT cells for cancer therapy. Building on previous studies, the overarching hypothesis to be tested in the Webb lab is that NKT cells play an important role in cancer immune surveillance and to address this hypothesis, her group aims to: 1. Determine the mechanisms by which NKT cells are reduced in cancer patients. 2. Design novel therapeutics to restore NKT cell number and function in cancer patients. 3. Investigate the mechanisms by which NKT cells recognize and destroy tumors.

One of Dr. Webb's main career goals is to be able to provide exceptional trainees with the opportunity to perform cutting edge research in an outstanding academic environment. In addition, research areas championed by her group include the development of novel cancer immunotherapeutic strategies and research into cancer health disparities.

Research/Clinical Keywords

cancer immunology, cancer immunotherapy, CD1d-mediated NKT cell activation, ELISA and flow cytometry

Highlighted Publications

Tiper IV, Temkin SM, Spiegel S, Goldblum SE, Giuntoli RL 2nd, Oelke M, Schneck JP, Webb TJ. VEGF Potentiates GD3-Mediated Immunosuppression by Human Ovarian Cancer Cells. Clin Cancer Res. 2016 Aug 15;22(16):4249-58.

Shissler SC, Bollino DR, Tiper IV, Bates JP, Derakhshandeh R, Webb TJ. Immunotherapeutic strategies targeting natural killer T cell responses in cancer Immunogenetics. 2016 Aug;68(8):623-38.

Webb TJ, Li X, Giuntoli RL 2nd, Lopez PH, Heuser C, Schnaar RL, Tsuji M, Kurts C, Oelke M, Schneck JP. Molecular identification of GD3 as a suppressor of the innate immune response in ovarian cancer. Cancer Res. 2012 Aug 1;72(15):3744-52. 

Webb TJ, Giuntoli RL 2nd, Rogers O, Schneck J, Oelke M. Ascites specific inhibition of CD1d-mediated activation of natural killer T cells. Clin Cancer Res. 2008 Dec 1;14(23):7652-8. 

Webb T.J., Litavecz R.A., Khan M.A., Du W., Gervay-Hague J., Renukaradhya G.J., Brutkiewicz R.R. (2006) Inhibition of CD1d1-mediated antigen presentation by the vaccinia virus B1R and H5R molecules. Eur J Immunol. 36(10): 2595-2600.

Webb, T.J., Sumpter, T.L., Thiele, A.T., Swanson, K.A., and Wilkes, D.S. (2005) The Phenotype and Function of Lung DCs. Crit Rev Immunol 25(6):465-91.



Additional Publication Citations

Tiper IV, Webb TJ. Histone deacetylase inhibitors enhance CD1d-dependent NKT cell responses to lymphoma. Cancer Immunol Immunother. 2016 Nov;65(11):1411-1421.

Webb TJ, Carey GB, East JE, Sun W, Bollino DR, Kimball AS, Brutkiewicz RR. Alterations in cellular metabolism modulate CD1d-mediated NKT-cell responses. Pathog Dis. 2016 Aug;74(6).

Younis RH, Han KL, Webb TJ. Human Head and Neck Squamous Cell Carcinoma-Associated Semaphorin 4D Induces Expansion of Myeloid-Derived Suppressor Cells. J Immunol. 2016 Feb 1;196(3):1419-29. 

Obata F, Subrahmanyam PB, Vozenilek AE, Hippler LM, Jeffers T, Tongsuk M, Tiper I, Saha P, Jandhyala DM, Kolling GL, Latinovic O, Webb TJ. Natural killer T (NKT) cells accelerate Shiga toxin type 2 (Stx2) pathology in mice. Front Microbiol. 2015 Apr 8;6:262.

Research Interests

aAPC-Mediated NKT cell Modulation to Enhance Cancer Immunotherapy

Natural killer T (NKT) cells comprise a specialized subset of T lymphocytes that express cell surface markers characteristic of NK cells. The ability of these cells to produce cytokines, activate cells of both the innate and adaptive immune responses, and recognize antigen in the context of CD1d molecules strongly suggest that NKT cells play a pivotal role in anti-tumor immunity. However, anti-tumor effects mediated by these cells may be compromised because cancer patients have a reduction in both NKT cell number and function. Therefore, we hypothesize that adoptive transfer of effector NKT cells will be an effective therapeutic strategy to enhance cancer immunotherapy. Our lab has developed CD1d-lg-based artificial Antigen Presenting Cells (aAPC), which can facilitate the induction and expansion of primary T and NKT cells. Research efforts are focused on modifying these CD1d-lg based aAPC to stimulate and analyze different NKT cell subsets in vitro and in vivo.


Restoring NKT cell function: a novel immunotherapeutic strategy for Breast Cancer

Preclinical studies and clinical trials have demonstrated that immunotherapy can effectively treat cancer; however, breast cancer immunotherapy needs to also focus on removing negative factors that could inhibit the immune response in order to maximize its therapeutic effects. The mechanisms by which NKT cells are functionally reduced in cancer patients have yet to be identified. It is known that lipids are frequently shed by tumors and can block immune responses. In fact, lipid levels are higher in the mammary tissue and sera of breast cancer patients compared to healthy controls. Thus, we hypothesize that lipid shedding by breast cancers cells is a mechanism used to inhibit NKT cell activation and possibly cause their death. Current studies are focused on investigating whether blocking breast cancer-associated ganglioside biosynthesis can restore NKT cell function.


Mechanisms by which ovarian cancers suppress CD1d-mediated NKT cell activation

Ovarian cancer is the fifth leading cause of cancer deaths among women, thereby accounting for more deaths than any other cancer of the female reproductive system.  It is known that ovarian cancer tissue and ascites contain lymphocytic infiltrates, suggesting that immune cells traffic to tumors, but are then inhibited by immunosuppressive molecules within the tumor microenvironment. Moreover, vascular endothelial growth factor (VEGF) expression is inversely correlated with survival in ovarian cancer patients.  Since avoiding detection by the host’s immune system is crucial for the growth and metastasis of cancer, we investigated the effects of ovarian cancer associated VEGF on CD1d-mediated antigen presentation to natural killer T (NKT) cells. Pretreatment of antigen presenting cells with ascites or conditioned medium from OV-CAR-3 and SK-OV-3 ovarian cancer cell lines suppressed CD1d-mediated NKT cell activation. Ovarian cancer-associated ascites and conditioned medium from ovarian cancer cell lines contain high levels of VEGF and ganglioside GD3.  Importantly, inhibiting VEGF production by ovarian cancer cell lines led to a reduction in GD3 expression and restored NKT cell activation. Thus, we have identified a novel link between immunosuppressive ganglioside shedding and VEGF production by ovarian cancers.  Current efforts are focused on determining the mechanisms by which VEGF signaling impairs CD1d mediated NKT cell responses, thus these studies have the potential to lead to the development of novel therapeutic targets for women with this disease. 

Lab Techniques and Equipment

The research in Dr. Webb's lab is focused on CD1d-mediated NKT cell activation and the assays used to monitor this interaction are typically qPCR, ELISA and flow cytometry. A variety of molecular techniques are also used to measure downstream signaling events and to modulate the function of proteins of interest.

Links of Interest