Angelina M. Bilate, Ph.D.

Post-Doc Researcher
Whitehead Institute for Biomedical Research
City, State
New York, NY
United States
Research Field
Award Year
Country Of Origin
Mentor Name
Juan Lafaille, Ph.D.


Experimental autoimmune encephalomyelitis (EAE) is a T-cell mediated disease of the central nervous system (CNS) used as model for multiple sclerosis. Afflicted mice show CNS inflammation, demyelination, and signs of paralysis, all of which bear similarities to patients with multiple sclerosis. The region of the CNS predominantly affected in most EAE models is the spinal cord but in some cases (e.g. in the absence of the inflammatory cytokine IFN, inflammation occurs preferentially in the cerebellum and brain stem. Dendritic cells (DC) are the most powerful antigen presenting cells (APC) for T cells, and it is these cells that enable effector immune responses to take place. Previous studies have shown that dendritic cells can be found in the CNS of mice afflicted with EAE; however, little is known about the nature and role of APCs in disease onset and progression. Lafaille et al (1994) developed an experimental model in which spontaneous EAE develops with an incidence of 100% in mice harboring a monoclonal T cell repertoire consisting of myelin basic protein (MBP)-specific T lymphocytes. The onset age of disease is quite predictable, making this model well suited for studying the sequence of events as healthy mice begin to develop disease. As T cells need to encounter and recognize antigen on the surface of an antigen presenting cell in order to trigger the disease, we sought to characterize the APC populations present in different regions of the CNS and analyze the proportions of different APCs before and after the onset of EAE in transgenic mice that develop spontaneous EAE. Our results showed that CD11b+ DCs were the predominant subtype found in the spinal cord of mice with acute EAE whereas plasmacytoid DC (pDC) were found mostly during chronic EAE, which coincides with the accumulation of regulatory T cells in the CNS. We also found the presence of small amounts of both of these DC populations in the CNS of young Tg/Tg mice (several weeks before the onset of EAE) and in non-transgenic mice, indicating that the DC compartment in healthy MBP-transgenic mice is similar to a wild-type mouse. The abundance of CD11b+ DCs is in agreement with the ability of this DC subset to stimulate the effector immune response. The next step will be to investigate whether pDCs are associated with regulation of EAE progression and which factors are required to maintain this particular DC subset in the CNS.