Abstract
Influenza claims hundreds of thousands of lives each year world wide. Unfortunately these numbers are relatively unchanged over the past few decades. Influenza vaccines work to prime the humoral immune response for subsequent challenges by the influenza virus. With this initial priming the humoral response will produce specific and highly effective antibodies for the given virus. While effective, the mechanisms of humoral memory formation and maintenance are relatively less explored than the cell mediated response. In primary infections, the innate response and CD8+ T-cells will often clear the bulk of the virus before the humoral response can produce a significant amount of antibody that we can track. In order to understand the humoral response and formation of humoral memory in primary and secondary challenges, we develop a model that tracks the response of its main components CD+ 4 T-cell, B Cells, and antibodies to the infection. We model B Cell memory formation through a mechanism triggered by the CD+ 4 T-Cell proliferation in order to examine conditions where memory formation is triggered. By fitting the model parameters to available data the model allows us to explore humoral system function in both normal and immune compromised systems.
Faculty Sponsors
Dr. Evan Haskell
Project Type
Event
Location
Alvin Sherman Library
Start Date
4-12-2013 1:00 PM
End Date
4-12-2013 5:30 PM
A B Cell Mediated Model of Humoral Immune System Function
Alvin Sherman Library
Influenza claims hundreds of thousands of lives each year world wide. Unfortunately these numbers are relatively unchanged over the past few decades. Influenza vaccines work to prime the humoral immune response for subsequent challenges by the influenza virus. With this initial priming the humoral response will produce specific and highly effective antibodies for the given virus. While effective, the mechanisms of humoral memory formation and maintenance are relatively less explored than the cell mediated response. In primary infections, the innate response and CD8+ T-cells will often clear the bulk of the virus before the humoral response can produce a significant amount of antibody that we can track. In order to understand the humoral response and formation of humoral memory in primary and secondary challenges, we develop a model that tracks the response of its main components CD+ 4 T-cell, B Cells, and antibodies to the infection. We model B Cell memory formation through a mechanism triggered by the CD+ 4 T-Cell proliferation in order to examine conditions where memory formation is triggered. By fitting the model parameters to available data the model allows us to explore humoral system function in both normal and immune compromised systems.
