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Title: How did they get there? Investigating how bacteria influence the establishment of lung resident T cells 

Abstract: The lung is a mucosal surface constantly exposed to insults from the outside world due to breathing. Because of this, the immune system in the lung must be poised to respond to these repeated insults quickly and thoroughly to eliminate any potential pathogenic threats. One of the potential pathogens that we often breathe in is Streptococcus pneumoniae (Spn). Our lungs accomplish rapid protection against this repeated exposure by calling for, and harboring, an important subset of immune cells called CD4⁺ tissue resident memory T cells (T_RM). These CD4⁺ T_RM cells provide frontline protection by quickly reactivating once they experience an Spn infection again. While these CD4⁺ T_RM cells have been shown to be critical in protection from Spn reinfection, it is unclear how Spn infections promote the establishment of these cells in the lungs initially. Spn induces an immune response through a variety of virulence factors, including a pore-forming toxin called pneumolysin (Ply), which causes host cell death and tissue damage to aid in its colonization and invasion. We were interested in whether Ply plays a role in influencing T_RM cell formation. In my dissertation work, I have been focused on understanding how Ply promotes T_RM cell formation in the lungs, and I will be discussing how that likely occurs and what implications this may have in understanding T_RM cell formation and function in the lung in comparison to other tissues. Our studies uncover an unexpected role for bacterial toxins in instructing T_RM cell establishment within mucosal tissues and have ramifications for development of the next generation CD4⁺ T_RM cell-directed anti-bacterial vaccines.