Heterologous Immunity
How Past Infections Shape Future Immune Responses
Our immune history influences how we respond to new infections—not just through classic antigen-specific memory, but also via TCR-independent responses. This mechanism may protect against unrelated infections or, in some contexts, exacerbate immune-mediated diseases.
Our work explores how innate acting T helper 1 (Th1) cells emerging from viral infections are maintained over time and activated during heterologous challenges. Using transcriptional and epigenetic data, we are identifying the key factors that regulate their responsiveness and plan to validate these candidates using genetic approaches.
In parallel, we examine bystander activation specifically in Th17 cells. Using a fungal infection model, we show that mice previously exposed to Candida albicans mount a stronger Th17 response to the unrelated fungus Malassezia, driven not by antigen recognition but by cytokine-mediated activation that leads to IL-17A production.
Together, our findings highlight how infection history can reprogram CD4 T cells to respond more broadly to future threats, revealing an additional layer of immune memory with important implications for infections and autoimmunity.
