How immune cells remember a natural pathogen varies depending on the route of infection, according to a report published this week online in Nature Immunology. The finding could affect vaccination strategies for achieving long-term immunologic protection in humans.
Marc Jenkins and colleagues assessed the generation and function of memory CD4+ T cells ― also called T helper cells ― in mice infected with bacteria that expressed a unique marker. This allowed the authors to count the number of those specific memory CD4+ T cells, thereby giving a more accurate measure of memory cell formation and longevity of these cells during a natural infection.
Infections occurring directly through the blood steam trigger more T cells that express the inflammatory molecule interferon-gamma (IFN-gamma), which helps to destroy host cells infected by the pathogen. Intranasal vaccination led to higher numbers of immune cells producing interleukin 17 (IL-17), which recruits more immune cells and triggers antimicrobial responses. Surprisingly, the IL-17-expressing immune cells are short-lived and wane several weeks after infection, whereas memory cells capable of producing IFN-gamma survived months longer.