A Mathematical Model of CR3/TLR2 Crosstalk in the Context of Francisella tularensis Infection

Rachel Leander
Mathematical Biosciences Institute, The Ohio State University

(February 16, 2012 10:30 AM - 11:30 AM)

A Mathematical Model of CR3/TLR2 Crosstalk in the Context of Francisella tularensis Infection

Abstract

Complement Receptor 3 (CR3) and Toll-like Receptor 2 (TLR2) are pattern recognition receptors ex- pressed on the surface of human macrophages. Although these receptors are essential components of the innate immune system, pathogen coordinated crosstalk between them can suppress the production of protective cytokines and promote infection. I will discuss a mathematical model of TLR2/CR3 crosstalk in the context of Francisella tularensis infection.