According to Dr Das: "I will keep the level of the talk at an introductory level where I will introduce the key players of our immune system and describe how they communicate and work together, ending with the key questions that remain to be understood. In the second talk I will be more specific show how mathematical modeling can help in understanding those questions in the context of T cell and NK cell signaling."

In the lung, alternatively activated macrophages (AAM) form the first line of defense against microbial infection. Due to the highly regulated nature of AAM, the lung can be considered as an immunosuppressive organ for respiratory pathogens. However, as infection progresses in the lung, another population of macrophages, known as classically activated macrophages (CAM) enters; these cells are typically activated by IFN-gamma. CAM are far more effective than AAM in clearing the microbial load, producing pro-inflammatory cytokines and anti-microbial defense mechanisms necessary to mount an adequate immune response. In this talk, I will outline the main differences between these two macrophage phenotypes, specifically in response to Mycobacterium tuberculosis (MTb) infection in the lung and present a mathematical model that determines the first time when the population of CAM becomes more dominant than the population of AAM. We call this event the “switching time” and use the model to propose strategies for reducing it.