Working Group in Pathogenic and Commensal Organisms
Organizers are Seth Michael Barribeau, David Schneider, Ann Tate, and Benjamin Sadd. With consequences for disease severity, resistance or clearance of a pathogen infection by an individual can be enhanced by a previous exposure to that pathogen, occurring either within an individual or even in its parents. This form of immune memory, traditionally thought the province of the vertebrate adaptive immune response, can also arise from innate immune pathways of vertebrates and invertebrates, and through distinct pathways in plants and bacteria. Researchers studying this phenomenon rarely interact across taxonomic boundaries, however, and use a preponderance of disparate terms to describe this innate immune mediated memory, including immune memory, immune priming, trained immunity, and systemic acquired resistance. This catalysis meeting will facilitate a synthesis of disparate researchers to better understand commonalities among these different forms of innate immune memory and key consequences for disease. They will use this opportunity to produce a broad interest synthesis manuscript elaborating upon specific avenues by which an improved understanding of innate immune memory will inspire future research, with direct and indirect benefits for human health. First, better understanding of how vertebrate immune memory works in retaining specific memory stands to improve vaccine design and delivery. Second, the specificity of immune memory could be manipulated to leave harmful pests, vectors, and human parasites susceptible to pathogen mediated biocontrol, while improving the health of beneficial organisms such as agricultural plants, animals, and pollinators that ensure human food security. Their approach aims to identify model systems functionally analogous to human innate immune memory that maximize our flexibility to interrogate the genetics, constraints, and functional manipulations of innate immune memory. Finally, this synthesis will elucidate fundamental concepts underlying host-pathogen evolution and the limits of immunological plasticity.
