Project description:We performed bulk RNA-sequencing analysis of brain and blood CD4+Foxp3+ Treg cells from sham and injured mice to characterize the gene expression profile of Tregs following traumatic brain injury and nasal anti-CD3 treatment
Project description:Bulk RNA-sequencing was performed to characterize the gene expression profile of microglia at acute and chronic timepoints following traumatic brain injury and nasal anti-CD3 treatment. We further investigated how the chronic microglial transcriptomic profile is modulated following traumatic brain injury and nasal anti-CD3 treatment in female mice with severe TBI, and in male mice with a delayed administration of treatment post-injury.
Project description:Bulk RNA-sequencing was performed to investigate the transcriptomic signature of phagocytic and non-phagocytic microglia following traumatic brain injury and nasal anti-CD3 treatment.
Project description:Investigating the impact of blocking the IL-10 receptor on the gene expression profile of microglia following chronic traumatic brain injury and nasal anti-CD3 treatment.
Project description:To determine the mechanism of regulation of Tregs by Setd2, LI Tregs (CD3+CD4+Foxp3-YFP+) from Setd2-deficient and control Tregs were subjected to RNA-seq analysis.
Project description:To determine the molecular regulation of Tregs by Setd2, spleen Tregs (CD3+CD4+Foxp3-YFP+) from Setd2-deficient and control Tregs were subjected to polII CUT&Tag analysis
Project description:To determine the molecular regulation of Tregs by Setd2, large intestine Tregs (CD3+CD4+Foxp3-YFP+) from Setd2-deficient and control Tregs were subjected to H3K27ac CUT&Tag analysis.
Project description:To determine the mechanism of regulation of Tregs by Setd2, SPTregs (CD3+CD4+Foxp3-YFP+) from Setd2-deficient and control Tregs were subjected to RNA-seq analysis.
Project description:We performed bulk RNA-seq from FACS-sorted Tregs (Foxp3+) and T convs (Foxp3-) CD4+ T cells from kidneys and spleens at different phases after injury.
Project description:The central nervous system (CNS) hypothalamus controls systemic metabolism. Inflammatory CNS processes evolving upon exposure to calorie-rich diet are thought to promote impaired metabolic CNS control, thereby triggering obesity and Type-2 diabetes (T2D). However, immune cells relevant for maintaining hypothalamic integrity remain incompletely understood. Here, we identify hypothalamic CD4+Foxp3+regulatory T(Treg) cells which control local tissue-inflammation. Specifically, upon exposure to a calorie-rich diet, a significant decline in hypothalamus-residing Foxp3+Tregs occurred and was accompanied by increased immune activation of CD4+T cells, infiltrating macrophages and microglia. Microglial proteomes of mice exposed to the hypercaloric challenge confirmed characteristics of immune activation; specifically, mRNA expression profiling of hypothalamic CD4+T cells indicated a Th1-mediated inflammatory state evidenced by high levels of Tbx21, Cxcr3, Cd226 and reduced expression of Ccr7 and S1P1 receptors relevant for recruitment to and retention at inflammatory sites. Using Treg depletion and transfer experiments in vivo, we found that Foxp3+Tregs critically limit hypothalamic immune activation induced by hyper-caloric challenge. Our findings open new avenues in the design of tailored concepts to improve immunometabolic health in obesity and T2D.
