The Role of Inflammation in Prostate Fibrosis and Urinary Dysfunction Using biological tools, we are embarking to determine if this is indeed the case, with the hopes of revealing potential ways to counteract viral pathogenesis.ĪSHLEE BELL-COHN, NORTHWESTERN UNIVERSITY In light of this, we hypothesize that a similar mechanism is taking place in human herpesviruses with the human homolog, the NKR-P1A/CD161 receptor. Strikingly, these ligands do not share a genetic origin, thus have evolved independently. Recently, the NKR-P1 family of NK receptors in rodents have been identified as targets of the beta-herpesvirus, cytomegalovirus (both rat and mouse), where they encode viral ligands that engage the inhibitory NKR-P1B receptor to evade NK detection. Many of these are inhibitory ligands that serve as decoys to evade immune recognition. Importantly, NK cells are key players in controlling herpesvirus infection and in recent years, many NK receptors have been found to directly interact with ligands expressed on virally-infected cells. They are tightly regulated by cell surface receptors, which can be either stimulatory or inhibitory, whose signals integrate to either activate or inhibit a given NK cell.
Natural killer (NK) cells are the first line of lymphocytes that respond to viral infections. The innate branch of the immune system plays a critical role in initiating appropriate immune responses to invading pathogens.
Investigating pathogen-driven evolution of the human Natural Killer (NK) receptor, NKR-P1A OSCAR ALBERTO AGUILAR, UNIVERSITY OF CALIFORNIA-SAN FRANCISCO
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