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Kathryn S. Jones, Ph.D.

Portait Photo of Kathryn Jones
Laboratory of Experimental Immunology
Leukocyte Biology Section
Staff Scientist (Contr)
Center for Cancer Research
National Cancer Institute
Building 567, Room 253
P.O. Box B
Frederick, MD 27102-1201
Phone:  
301-846-5262
Fax:  
301-846-7034
E-Mail:  
joneska@mail.nih.gov

Biography

Dr. Kathryn Jones is a principal scientist with SAIC-Frederick working in collaboration with the Laboratory of Experimental Immunology. She obtained her Ph.D. from Albert Einstein College of Medicine, working on the pathogenicity of murine retroviruses under Frank Lilly. She did her post-doctoral fellowship on retroviral integrase proteins with Anna Marie Skalka at Fox Chase Cancer Center. Dr. Jones worked at the University of Maryland School of Medicine and VA Medical Center in Baltimore before joining NCI in 1996.

Research

The focus of our research over the past several years has been the viral and cellular factors involved in transmission, persistence and pathogenesis of HTLV-1. Although it has been known for many years that HTLV-1 infects CD4+ T cells, neither the molecules in the receptor complex on these cells nor the identity of other cell types involved in viral spread have been well defined. Moreover, little is known about the role of innate and adaptive immunity in the persistence or pathogenesis of this virus.

One specific goal of this work has been to investigate whether cells other than CD4+ T cells are involved in the transmission and/or pathogenesis of HTLV-1. Unlike most other retroviruses, cell-free HTLV-I virus particles cannot productively infect its primary target cell (CD4+ T cells) in vitro. We recently reported that, unlike T cells, dendritic cells (DC) are efficiently infected following exposure to cell-free HTLV-I virions. Moreover, DCs exposed to HTLV-I can rapidly, efficiently and reproducibly transfer virus to autologous primary CD4+ T cells. These studies, along with observations that HTLV-I-infected DC are present in HTLV-1-infected individuals, indicate that infected DC play an important role in the spread of this virus. Since infection of DC cells by other viruses have been shown to contribute to persistence and/or pathogenesis, we are examining dendritic cells infected in vitro as well as dendritic cells isolated from HTLV-1-infected individuals to determine whether DC function is impaired.

Another goal of our work has been to identify the molecules on primary T cells and other immune cells involved in transmission, and to understand on the molecular level the interactions between the HTLV envelope proteins and these cellular receptors. Several years ago, we reported that heparan sulfate proteoglycans (HSPGs) were critical for efficient binding and entry of HTLV-I into CD4+ T cells. More recently, we have observed that HSPGs are also involved in the infection of DC, and the DC-mediated infection of CD4+ T cells. Currently, we are investigating interactions between HSPGs and another molecule involved in HTLV-I entry, Neuropilin-1, during virus binding and infection. Since many retroviruses downregulate their receptors after infection of a cell, we are also investigating whether these molecules play a role in the cellular tropism and/or the pathobiology of HTLV-I.

This page was last updated on 4/9/2014.