A pair of studies examining immune response in C. elegans reveal broad implications for understanding pathogen detection in higher animals and the evolutionary origins of immunity itself. The research, co-authored by MD/Ph.
D. student Samantha "Sammy" Tse-Kang and Read Pukkila-Worley, MD, professor of medicine, uncovered a mechanism of effector-triggered immunity in animals, in which host cells detect infection by sensing the harmful effects of a pathogen rather than simply the presence of a dangerous microbe. The new research details the mechanism of an immune regulator whose role in pathogen sensing is conserved across all organisms.
The papers, which were published simultaneously in the journals Immunity and Cell Reports , examine a type of immune regulator called SARM, which is required for immune defenses in plants and bacteria. It was not previously known whether these proteins have a role in pathogen sensing in animals. Tse-Kang and her colleagues showed that the SARM homolog in C.
elegans is specifically expressed on a cellular compartment in intestinal cells that enables it to respond to pathogen-induced damage to the host and activate protective immune defenses. Tse-Kang said the two papers began with a single question: "What regulates the immune response in C. elegans?" "These companion papers started from an unbiased genetic screen, and it was not always clear where these stories were progressing.
As we went along, we realized that we were thinking about two separa.