We use basic immunology principles to develop mechanistic models of immunity, simulate the progression of an immune response following vaccination or infection, and determine potential mechanisms of protection that underlie empirical observations (e.g., correlates of protection) identified in vaccine clinical studies. Specifically, we use a chemical kinetics-based approach to model 1) cellular and innate immunity, 2) B cell affinity maturation, and 3) antibody-based binding and neutralization.
Chaudhury, S., J. A. Regules, C. A. Darko, S. Dutta, A. Wallqvist, N. C. Waters, E. Jongert, F. Lemiale, and E. S. Bergmann-Leitner. Delayed fractional dose regimen of the RTS,S/AS01 malaria vaccine candidate enhances an IgG4 response that inhibits serum opsonophagocytosis. Scientific Reports. 2017 August 11; 7:7998. [PDF]
Ripoll, D. R., I. Khavrutskii, A. Wallqvist, and S. Chaudhury. Modeling the role of epitope arrangement on antibody binding stoichiometry in flaviviruses. Biophysical Journal. 2016 October 18; 111(8):1641-1654. [PDF]
Chaudhury, S., J. Reifman, and A. Wallqvist. Simulation of B cell affinity maturation explains enhanced antibody cross-reactivity induced by the polyvalent malaria vaccine AMA1. Journal of Immunology. 2014 September 1; 193(5):2073-2086. [PDF]