The lab’s primary interest is identifying viral and host factors that promote maladaptive interferon (IFN) responses and contribute to the development of immunopathologies. IFNs are critical for the establishment of antiviral responses and must be carefully regulated to balance curbing pathogen dissemination and avoiding the induction of deleterious responses. These responses are often associated with autoinflammation, irreversible tissue damage, and enhanced viral disease severity.
We favor an interdisciplinary approach to understanding the molecular basis for innate immune recognition, the regulation of IFN synthesis and the establishment of an antiviral state. We are delineating the signal transduction cascades control expression and activation state of interferon regulatory factors (IRFs), key transcriptional activators that coordinate the antiviral gene expression programs. These responses are thought to be triggered ubiquitously across tissues. Thus, we are interested in understanding the contribution of cell-identity to the protective and potentially harmful effects of an unabated innate immune response. This will reveal tissue-specific vulnerabilities in signal transduction cascades targeted by pathogens or disrupted in autoimmune and proliferative diseases, which can be exploited for the management of deleterious inflammation.
740 Biomedical Research Tower (BRT)
460 W 12th Ave, Columbus OH 43210
Noushin Saljoughian Esfahani, Research Associate, firstname.lastname@example.org