Project description:During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each. Naive CD44Lo CD8+ T cells were isolated and sorted from uninfected C57BL/6 mice and H2-Db GP33-specific CD8+ T cells were sorted using MHC-I tetramers at d6, 8, 15, and 30 p.i. with either LCMV Arm or LCMV clone 13. RNA from these CD8+ T cells was processed, amplified, labeled, and hybridized to Affymetrix GeneChip MoGene 1.0 st microarrays
Project description:During acute viral infections, naïve CD4+ T cells differentiate into effector CD4+ T cells and, after viral control, into memory CD4+ T cells. Memory CD4+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD4+ T cells become less functional. To compare the development of functional memory T cells with poorly functional T cells from chronic viral infection, we generated longitudinal transcriptional profiles for each. Naive CD44Lo CD4+ T cells were isolated and sorted from uninfected C57BL/6 mice and H2-IAb GP66-specific CD4+ T cells were sorted using MHC-II tetramers at d6, 8, 15, and 30 p.i. with either LCMV Arm or LCMV clone 13. RNA from these CD4+ T cells was processed, amplified, labeled, and hybridized to Affymetrix GeneChip MoGene 1.0 st microarrays.
Project description:During acute viral infections, naïve CD4+ T cells differentiate into effector CD4+ T cells and, after viral control, into memory CD4+ T cells. Memory CD4+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD4+ T cells become less functional. To compare the development of functional memory T cells with poorly functional T cells from chronic viral infection, we generated longitudinal transcriptional profiles for each.
Project description:During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each.
Project description:The profiles of H3K27 tri-methylation in CD8+ T cells from LCMV-Armstrong and LCMV-Clone 13 infected mice are known to be distinct from one another. We used CUT&RUN (Cleavage Under Targets and Release Using Nuclease) to analyze these differences in splenic CD8+ T cells of these two infection conditions.
Project description:The transcriptomes of CD8+ T cells from LCMV-Armstrong and LCMV-Clone 13 infected mice are known to be distinct from one another. We used single cell RNA sequencing (scRNA-seq) to analyze the transcriptomic diversity of splenic CD8+ T cells in these two infection conditions at various timepoints after infection.
Project description:The profiles of open chromatin regions of CD8+ T cells from LCMV-Armstrong and LCMV-Clone 13 infected mice are known to be distinct from one another. We used Assay for Transposase-Accessible Chromatin using sequencing at the single cell level (scATAC-seq) to analyze these differences in splenic CD8+ T cells of these two infection conditions at Division 1 post-infection.
Project description:Chronic but not acute infections cause cachexia, characterized by bodyweight reduction and muscle loss. The underlying mechanisms remain incompletely understood. It is also not clear if muscle, in turn, regulates antiviral immune responses. In this study, we use two infection mouse models, one is acute and the other is chronic (described in PMID6332167 and PMID17950003), to study the global transcript profiles in muscles during infections.