Minelva R Nanton
Affiliation: University of Minnesota
- Cutting edge: B cells are essential for protective immunity against Salmonella independent of antibody secretionMinelva R Nanton
Department of Pediatric Infectious Disease, Center for Infectious Diseases and Microbiology Translational Research, University of Minnesota Medical School Twin Cities, Minneapolis, MN 55455, USA
J Immunol 189:5503-7. 2012..Taken together, these data suggest that the primary role of B cells in acquired immunity to Salmonella is via the development of protective T cell immunity...
- Direct visualization of endogenous Salmonella-specific B cells reveals a marked delay in clonal expansion and germinal center developmentMinelva R Nanton
Center for Comparative Medicine, Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California Davis, Davis, CA, USA Microbiology, Immunology, and Cancer Biology Graduate Program, University of Minnesota Medical School Twin Cities, Minneapolis, MN, USA
Eur J Immunol 45:428-41. 2015..Together, these data suggest that Salmonella can simultaneously inhibit host B- and T-cell responses using SPI2-dependent mechanisms. ..
- Innate immune activation during Salmonella infection initiates extramedullary erythropoiesis and splenomegalyAmy Jackson
Center for Infectious Diseases and Microbiology Translational Research, Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455, USA
J Immunol 185:6198-204. 2010..These data indicate that early innate immunity to Salmonella initiates marked splenic erythropoiesis and may hinder bacterial clearance...
- Selective culling of high avidity antigen-specific CD4+ T cells after virulent Salmonella infectionJames M Ertelt
Department of Pediatrics, University of Minnesota School of Medicine, Center for Microbiology and Infectious Disease Translational Research, Minneapolis, MN 55455, USA
Immunology 134:487-97. 2011..Hence, virulent Salmonella triggers the selective culling of high avidity activated CD4+ T-cell subsets, which re-shapes the repertoire of antigen-specific T cells that persist later after infection...