Pathogen size alters C-type lectin receptor signaling in dendritic cells to influence CD4 T cell differentiation

A key mechanism to eliminate pathogens from the body is the physical internalization (phagocytosis) and degradation of microbes by specialized cells of the immune system including neutrophils, macrophages, and dendritic cells. Phagocytosis not only eliminates potentially harmful pathogens, but also provides information about the “type” of microbe encountered, and helps to orchestrate an appropriate adaptive immune response. Certain pathogens, including filamentous fungi and parasite worms (helminths), exceed the size limit for phagocytosis. In this study we show that when dendritic cells encounter pathogens that are too large to internalize, or when phagocytosis of small microbes is blocked, dendritic cells adopt an activation profile that allows them to orchestrate an adaptive immune response commonly associated with tissue repair and anti-helminth immunity. Overall design: Examination of mice bone marrow derived dendritic cell behavior with different physical forms of C.albicans