Tbet expression by Tregs is needed to protect against Th1-mediated immunopathology during Toxoplasma infection in mice
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ABSTRACT:
PROVIDER: PRJNA761772 | ENA |
REPOSITORIES: ENA
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Project description:Tregs dynamically respond to the inflammatory environment by acquiring features of the inflammatory cells they regulate. This is called Treg plasticity. We aimed to understand how Treg plasticity impacts the immune response to the protozoan parasite, T. gondii during the acute infection phase in the mouse model. Our study provides unique information of how plasticity of Tregs positivily impacts the overall fitness of the Treg during an infection.
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Project description:The role of antibody and B cells in preventing infection is established. In contrast, the role of B cell responses in containing chronic infections remains poorly understood. IgG2a (IgG1 in humans) can prevent acute infections and T-bet promotes IgG2a isotype switching. However, whether IgG2a and B cell-expressed T-bet influence the host-pathogen balance during persisting infections is unclear. Here we demonstrate that B cell specific loss of T-bet prevents control of persisting viral infection. T-bet in B cells not only controlled IgG2a production, but also mucosal localization, proliferation, glycosylation, and a broad transcriptional program. T-bet controlled a broad antiviral program in addition to IgG2a since T-bet in B cells was imÂportant even in the presence of virus-specific IgG2a. Our data supports a model in which T-bet is a universal controller of antiviral immunity across multiple immune lineages. Naïve, Tbet+, and Tbet- Memory B cells were assayed for gene expression Tbet GFP reporter mice were infected with LCMV clone 13, and target B cell populations were sorted from splenocytes at day 10 post-infection
2016-08-01 | E-GEOD-81189 | biostudies-arrayexpress
Project description:Clinically, obesity is strongly associated with severe TH2 immunopathology, though the physiological, cellular, and molecular underpinnings of this association remain obscure. We demonstrate that obese mice are susceptible to severe atopic dermatitis (AD), a major manifestation of TH2 immunopathology and disease burden in humans. Mechanistically, we show that dysregulation of the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARg) in T cells is a causal link between obesity and the increased TH2 immunopathology. We find that PPARg directly controls a cellular metabolic transcriptional program that restrains nuclear gene expression of the chief TH2 effector cytokines interleukin-4 (IL-4) and interleukin-13 (IL-13). Accordingly, thiazolidinediones (TZDs), potent PPARg agonists, robustly protect obese mice from TH2 immunopathology. Collectively, these findings establish PPARg as a molecular link between obesity and TH2 immune homeostasis and identify TZDs as novel therapeutic candidates for TH2 immunopathology.
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Project description:By RNA-sequencing, we compared four different bone marrow (BM)-derived Tregs, and found that the gene expression profile from No Tumor transplanted group and ST2-KO Tregs tansplanted group shown similar pattern, while WT Treg and Tbet-KO Tregs transplanted group shown the similar trend.
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Project description:CD4 T cells promote innate and adaptive immune responses, but how vaccine-elicited CD4 T cells contribute to immune protection remains unclear. Here we evaluated whether induction of virus-specific CD4 T cells by vaccination would protect mice against infection with chronic lymphocytic choriomeningitis virus (LCMV). Immunization with vaccines that selectively induced CD4 T cell responses resulted in catastrophic inflammation and mortality following challenge with a persistent form of LCMV. Immunopathology required antigen-specific CD4 T cells and was associated with a cytokine storm, generalized inflammation, and multi-organ system failure. Virus-specific CD8 T cells or antibodies abrogated the pathology. These data demonstrate that vaccine-elicited CD4 T cells in the absence of effective antiviral immune responses can trigger lethal immunopathology. Splenic GP66-specific CD4 T cells from mice immunized with either a LMwt vaccine (sham) or LMgp61 vaccine (CD4 vaccine) were purified by FACS on day 8 post-infection with LCMV clone 13
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Project description:To investigate the role of Tbet in B cell differentiation to "effector-like" antibody secreting cells (ASC's) we utilized an ex vivo culture system to differentiate B cells in the presence of Th1 (Be1) or Th2 (Be2) polarized T cells. To determine the role of Tbet in Be1 cell differentiation we performed ATAC-seq on Wt Be1 and Tbet negative (TbetNeg) Be1 cells and Wt Be2 and Tbet negative (TbetNeg) Be2 cells. Collectively, these data show that T-bet serves as master regulator for the Be1 cell fate and is required to program chromatin accessibility during ASC differentiation in Be1 cells.
2019-04-29 | GSE118984 | GEO
Project description:Inflammatory (B220+ CD19+ CD44+ CD11c+ Tbet-AmCyanhi) B cells were sorted from female Tbet-AmCyan reporter mice at day 8, 10, and 15 post infection with LCMV-Armstrong. RNA-seq was employed to assess transcriptional changes in inflammatory B cells throughout the infection.
2022-01-27 | GSE192765 | GEO
Project description:Inflammatory (B220+ CD19+ CD44+ CD11c+ Tbet-AmCyanhi) B cells were sorted from female Tbet-AmCyan reporter mice at day 8, 10, and 15 post infection with LCMV-Armstrong. RNA-seq was employed to assess transcriptional changes in inflammatory B cells throughout the infection.
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Project description:T-bet and Eomes are related T-box transcription factors that control NK cell development. This study was designed to understand the specific roles of Eomes and T-bet in regulating gene expression. RNAseq data were generated for immature (CD11b- CD27+) and mature (CD11b+ CD27-) NK cells from T-bet KO (Tbet Ho) or control mice (Tbet WT) or from Eomes KO (Eomes Ho) or control mice (NK-Cre). Three samples were generated for each condition (Tri 1, 2, 3).
2021-05-10 | GSE168240 | GEO