Thomas E. Lane
Molecular Biology & Biochemistry
School of Biological Sciences
Phone: (949) 824-5878
Email: tlane@uci.edu
http://darwin.bio.uci.edu/~faculty/lane/
http://www.faculty.uci.edu/profile.cfm?faculty_id=4468
Thomas Lane
The major focus of work in Dr. Lane’s laboratory is to better understand the underlying immunopathological mechanisms involved in virus-induced central nervous system (CNS) disease. Infection of susceptible mice with neuroadapted strains of mouse hepatitis virus (MHV) results in an acute encephalitis followed by a chronic, progressive demyelinating disease with many clinical and histologic similarities with the human demyelinating disease Multiple Sclerosis (MS). As such, the MHV-mouse model is considered a relevant model for MS. Although the mechanism(s) which contribute to demyelination in MHV-infected mice have not been fully defined, it is thought that the immune response plays a critical role in contributing to disease. In support of this are a recent series of studies from my laboratory that have demonstrated the importance of CD4+ T cells and macrophages to myelin destruction.
In related work, they have evaluated the functional significance of chemokine expression within the CNS of mice following infection with MHV. In brief, they have conclusively determined that expression of these proinflammatory molecules contributes not only to host defense but also disease development by attracting targeted populations of leukocytes at defined times post-infection with virus. They are continuing their investigations of the importance of chemokines as they relate to viral infection of the CNS. These studies have broad-range implications with regards to understanding the biology of this diverse family of proteins and may offer insights to other human diseases, including cancer.
Selected Publications:
Deane, J. A., Kharas, M. G., Oak, J. S., Stiles, L. N., Luo, J., Moore, T. I., Ji, H., Rommel, C., Cantley, L. C., Lane, T. E., and Fruman, D. A. (2007). T-cell function is partially maintained in the absence of class IA phosphoinositide 3-kinase signaling. Blood 109(7), 2894-2902.
Held, K. S., Glass, W. G., Orlovsky, Y. I., Shamberger, K. A., Petley, T. D., Branigan, P. J., Cunningham, M. R., Benson, J. M., and Lane, T. E. (2007). Antibody blocking of IL-12/23 ameliorates autoimmune but not viral-induced encephalomyelitis. Journal of Neurovirology 13, 84-84.
Ramos, S. J., Hardison, J. L., Stiles, L. N., Lane, T. E., and Walsh, C. M. (2007). Anti-viral effector T cell responses and trafficking are not dependent upon DRAK2 signaling following viral infection of the central nervous system. Autoimmunity 40(1), 54-65.
Schaumburg , C. S., Gatzka, M., Walsh, C. M., and Lane, T. E. (2007). DRAK2 regulates memory T cell responses following murine coronavirus infection. Autoimmunity 40(7), 483-488.
Walsh, K. B., Lanier, L. L., and Lane, T. E. (2008). NKG2D receptor signaling enhances cytolytic activity by virus-specific CD8(+) T cells: Evidence for a protective role in virus-induced encephalitis. Journal of Virology 82(6), 3031-3044. |
