Innate immune pathways are found as far back as early branching metazoans, however these pathways have evolved extensively and become increasingly complex in higher organisms. Indeed, the innate immune system is known to defend against invading pathogens via a suite of germline encoded pattern recognition receptors (PRRs) that detect pathogen- associated molecular patterns (PAMPs) —highly invariable components of microbial origin, to activate proinflammatory and other innate immune gene programs that lead to pathogen elimination. Emerging studies underscore the complexities of innate immunity, revealing that certain PRRs additionally serve as sensors of damage- associated molecular patterns (DAMPs) —endogenous ligands generated during the course of tissue damage, injury, or genetic disease. In this context, a heightened and dysregulated innate immune response in the absence of infection can trigger and sustain autoimmune and inflammatory disease pathology. Accordingly, mounting evidence demonstrates that cytosolic detection of aberrant self-DNA species via select PRRs represents a pivotal common pathway in driving multiple inflammatory disease states. Our laboratory is interested in understanding innate immune pathways and the mechanisms by which nucleic acid sensing PRRs propagate the inflammatory response with an overall goal to develop the next generation of therapeutics to combat microbial infections and treat autoinflammatory disorders.
To view Dr. Parvatiyar's publications see Pubmed.