Abstract

Cervical cancer is caused by infection with high-risk human papillomaviruses (HPVs). The viral etiology of this cancer indicates that it should be possible to develop highly specific and effective antiviral and antitumor vaccines. The control of HPV infection and associated lesions is believer to be mediated through the action of cytotoxic T cells (CTLs). The only small animal model for the study of high risk (cancer-associated) papillomavirus infection is the cottontail rabbit papillomavirus (CRPV)-rabbit model. Using this model, my laboratory has produced a number of CRPV vaccines that protect rabbits against primary CRPV infection or that suppress the clinical manifestations of a preestablished infection. Our ability to advance beyond the current in vivo results is hindered by the fact that a CTL assay for rabbits is currently not available. Since recent advances in immunology make it feasible to develop a rabbit CTL assay, this is the goal of our project.
Our specific aims are: 1) to produce a source of immortal cells for the development of CTL targets; 2) to generate antigen-specific target cells; 3) to develop a CTL assay using effector cells from vaccinated rabbits.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
5P30AR041942-07
Application #
6318510
Study Section
Special Emphasis Panel (ZAR1-AAA-C (J1))
Project Start
1992-09-30
Project End
2004-03-31
Budget Start
Budget End
Support Year
7
Fiscal Year
2000
Total Cost
$72,259
Indirect Cost

  Institution

Name
Yale University
Department
Type
DUNS #
082359691
City
New Haven
State
CT
Country
United States
Zip Code
06520

  Publications

Dainichi, Teruki; Hayden, Matthew S; Park, Sung-Gyoo et al. (2016) PDK1 Is a Regulator of Epidermal Differentiation that Activates and Organizes Asymmetric Cell Division. Cell Rep 15:1615-23
Askenase, Phillip W; Bryniarski, Krzysztof; Paliwal, Vipin et al. (2015) A subset of AID-dependent B-1a cells initiates hypersensitivity and pneumococcal pneumonia resistance. Ann N Y Acad Sci 1362:200-14
Clark, Paul R; Jensen, Todd J; Kluger, Martin S et al. (2011) MEK5 is activated by shear stress, activates ERK5 and induces KLF4 to modulate TNF responses in human dermal microvascular endothelial cells. Microcirculation 18:102-17
Kwong, Bernice Y; Roberts, Scott J; Silberzahn, Tobias et al. (2010) Molecular analysis of tumor-promoting CD8+ T cells in two-stage cutaneous chemical carcinogenesis. J Invest Dermatol 130:1726-36
Radtke, Christine; Vogt, Peter M; Devor, Marshall et al. (2010) Keratinocytes acting on injured afferents induce extreme neuronal hyperexcitability and chronic pain. Pain 148:94-102
Kirkiles-Smith, Nancy C; Harding, Martha J; Shepherd, Benjamin R et al. (2009) Development of a humanized mouse model to study the role of macrophages in allograft injury. Transplantation 87:189-97
Koga, Yasuo; Pelizzola, Mattia; Cheng, Elaine et al. (2009) Genome-wide screen of promoter methylation identifies novel markers in melanoma. Genome Res 19:1462-70
Yates, Kristin E; Korbel, Gregory A; Shtutman, Michael et al. (2008) Repression of the SUMO-specific protease Senp1 induces p53-dependent premature senescence in normal human fibroblasts. Aging Cell 7:609-21
Pelizzola, Mattia; Koga, Yasuo; Urban, Alexander Eckehart et al. (2008) MEDME: an experimental and analytical methodology for the estimation of DNA methylation levels based on microarray derived MeDIP-enrichment. Genome Res 18:1652-9
Shen, Xiaoyan; Berger, Carole L; Tigelaar, Robert et al. (2008) Development of immunogenic tumor-loaded dendritic cells through physical perturbation and apoptotic cell loading. Immunol Invest 37:798-821

Showing the most recent 10 out of 97 publications