Our lab is broadly interested in understanding more about the interplay between infection, inflammation, and red blood cell biology.
Erythroid progenitors express several pattern recognition receptors that are capable of detecting microbial infection. We are interested in exploring the molecular mechanisms that erythroid progenitors use to mount an innate antiviral immune response.
Chronic inflammation triggered by infection, autoimmunity, or inflammatory disorders can lead to a decrease in the production and survival of mature RBCs known as anemia of inflammation. The mechanisms that lead to anemia of inflammation are poorly defined. We hypothesize that activation of nucleic acid sensors in erythroid progenitors may alter the function and differentiation of their mature RBC descendants.
Mammals are the only vertebrates that discard their organelles during erythropoiesis. Nucleated red blood cells in non-mammalian vertebrates are immunologically active. We aim to identify and explore conserved immune mechanisms of vertebrate erythroid cells.