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Transcriptional profiling of Follicular B cells (FoB) in control and T follicular regulatory cell deficient mice

ABSTRACT: We isolated Follicular B cells from naïve and Brucella infected mice to determine how T follicular regulatory cells alter the B cell response to infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE231772 | GEO | 2023/08/31

REPOSITORIES: GEO

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Transcriptional profiling of Follicular B cells (FoB) in control and T follicular regulatory cell deficient mice

Project description:Transcriptional profiling of Follicular B cells (FoB) in control and T follicular regulatory cell deficient mice

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Germinal centers continually recruit naïve T cells that alter the balance between follicular T helper and follicular regulatory T cells.

Project description:Germinal centers continually recruit naïve T cells that alter the balance between follicular T helper and follicular regulatory T cells.

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Follicular B (FoB) cells purified from miR-17-92 transgenic mice

Project description:We have generated a miR-17-92 transgenic allele (termed miR-17-92 Tg) whose expression can be turned on conditionally by Cre recombinase (Xiao et al, Nature Immunology, 9:405-14, 2008). The mice were crossed to CD19-Cre mice to turn on the transgene expression specifically in B cells. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 Tg/Tg mice (FoBtg1, FoBtg2, FoBtg3) and miR-17~92 Tg/Tg mice (FoBwt1, FoBwt2, FoBwt3) by MACS depletion of cells positive for CD5, CD43, and CD93 (also known as AA4.1). The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2011-07-21 | E-GEOD-30877 | biostudies-arrayexpress

Follicular B (FoB) cells purified from miR-17-92 tKO mice

Project description:We have generated a miR-17~92 fl/fl allele whose expression can be turned off conditionally by Cre recombinase in the miR-106a-363-/-;miR-106b-25-/- background. The mice were crossed to CD19-Cre mice to turn off the expression of miR-17~92 specifically in B cells. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 fl/fl;miR-106a-363;miR-106b~25 mice (tKO1, tKO2, tKO3) and CD19-cre (Control1, Control2, Control3) by MACS depletion of cells positive for CD9, CD43, and CD93 (also known as AA4.1). The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

2014-04-01 | E-GEOD-56376 | biostudies-arrayexpress

Germinal centers continually recruit naïve T cells that alter the balance between follicular T helper and follicular regulatory T cells.

Project description:Follicular helper T cells (T FH ) mediate B cell selection and clonal expansion in germinal centers (GCs), and follicular regulatory T cells (T FR ) prevent the emergence of self-reactive B cells and help to extinguish the reaction. Here we show that GC reactions continually recruit T cells from both the naïve conventional and naive thymic regulatory T cell (Treg) repertoires. In the early GC, newly recruited T cells develop into T FH , whereas cells entering during the contraction phase develop into T FR cells that contribute to GC dissolution. The T FR fate decision is associated with decreased antigen availability and is modulated by slow antigen delivery or mRNA vaccination. Thus, invasion of ongoing GCs by newly developing T FH and T FR from naïve conventional and Treg repertoires, helps remodel the GC based on antigen availability.

2023-08-19 | GSE240730 | GEO

Differential gene expression profiling of conventional (Tconv), regulatory (Treg), follicular (TFH) helper and follicular regulatory (TFR) T-cells from control vs OX40L-Jagged-1 treated NZBWF1/j mice

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Follicular B (FoB) cells purified from miR-17-92 tKO mice, stimulated with LPS/IL-4, 13.5hr

Project description:We have generated a miR-17~92 fl/fl allele whose expression can be turned off conditionally by Cre recombinase in the miR-106a-363-/-;miR-106b-25-/- background. The mice were crossed to CD19-Cre mice to turn off the expression of miR-17~92 specifically in B cells and stimulated LPS/IL-4 for 13.5hr. Follicular B(FoB) cells were purified from CD19-Cre;miR-17~92 fl/fl;miR-106a-363;miR-106b~25 mice (TKO1, TKO2, TKO3) and WT (WT1, WTl2, WT3) by MACS depletion of cells positive for CD9, CD43, and CD93 (also known as AA4.1). The purified B cells were stimulated with LPS/IL-4 for 13.5hr in B cell media. The purity of follicular B cells was examined by flow cytometry and was greater than 95% for all samples. Total RNA was extracted using RNeasy kit (QIAGEN).

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Brucella melitensis-infected HeLa cells gene expression

Project description:In a time course study, we characterized global gene expression profile of B. melitensis-infected epithelium-like cells at the onset of infection. B. melitensis-infected HeLa cells exhibited a down-regulated expression profile at 4 h (48 up- and 109 down-regulated genes) that transitioned to an activated transcriptional profile at 12 h post-infection (733 up- and 224 down-regulated genes). The analysis of the results indicates that infected cells undergo an adaptation period during the first 4 h p.i. that is overcome by 12 h p.i., permitting Brucella to replicate intracellularly while minimally affecting host physiological processes. Specific genes and biological processes identified in this study will further help elucidate how both host and Brucella interact during the early infectious process to the eventual benefit of the pathogen and to the detriment of the naïve host. Keywords: Time course study of gene expression profile of Brucella melitensis-infected HeLa cells

2012-12-27 | GSE14703 | GEO

CXCR5+ follicular cytotoxic T cells control viral infection in B cell follicles

Project description:In response to infection, antigen-specific CD8+ T cells are primed in the T cell zone of secondary lymphoid organs and differentiate into cytotoxic effector T (TC) cells. Concurrently, CD4+ T cells differentiate into follicular helper T (TFH) cells that localize to B cell follicles and promote protective antibody responses. During unresolved infections, however, some viruses including human immunodeficiency virus (HIV) or Epsteinâ??Barr virus (EBV) escape immune control and persist in TFH cells and B cells, respectively. Exclusion of Tc cells from B cell follicles is thought to be a major mechanism of immune evasion. New strategies are therefore needed to eradicate infected cells in follicles for a permanent cure. Using mouse infection models and human samples, we here identify a specialized group of TC cells expressing the chemokine receptor CXCR5 that can selectively enter B cell follicles and eradicate infected TFH and B cells. We demonstrate that differentiation of these cells, which we term follicular cytotoxic T (TFC) cells, requires the transcription factors Bcl6, E2A and Tcf1, whereas the transcriptional regulators Blimp1, Id3 and Id2 inhibit their development. We demonstrate that Blimp1 and E2A directly regulate Cxcr5 expression, and together with Bcl6 and Tcf1 form a transcriptional circuit that guides the TFC differentiation. The identification of a follicular subset of TC cells has far reaching implications for developing better strategies for the control of infections that target B cells and TFH cells and for the eradication of B cell derived malignancies. There is no associated input. The E2A Bio-ChIP-seq was performed with total thymocytes from Tcf3Bio/Bio Rosa26BirA/BirA mice

2016-08-01 | E-GEOD-84974 | biostudies-arrayexpress

CXCR5+ follicular cytotoxic T cells control viral infection in B cell follicles

Project description:In response to infection, antigen-specific CD8+ T cells are primed in the T cell zone of secondary lymphoid organs and differentiate into cytotoxic effector T (TC) cells. Concurrently, CD4+ T cells differentiate into follicular helper T (TFH) cells that localize to B cell follicles and promote protective antibody responses. During unresolved infections, however, some viruses including human immunodeficiency virus (HIV) or Epstein–Barr virus (EBV) escape immune control and persist in TFH cells and B cells, respectively. Exclusion of Tc cells from B cell follicles is thought to be a major mechanism of immune evasion. New strategies are therefore needed to eradicate infected cells in follicles for a permanent cure. Using mouse infection models and human samples, we here identify a specialized group of TC cells expressing the chemokine receptor CXCR5 that can selectively enter B cell follicles and eradicate infected TFH and B cells. We demonstrate that differentiation of these cells, which we term follicular cytotoxic T (TFC) cells, requires the transcription factors Bcl6, E2A and Tcf1, whereas the transcriptional regulators Blimp1, Id3 and Id2 inhibit their development. We demonstrate that Blimp1 and E2A directly regulate Cxcr5 expression, and together with Bcl6 and Tcf1 form a transcriptional circuit that guides the TFC differentiation. The identification of a follicular subset of TC cells has far reaching implications for developing better strategies for the control of infections that target B cells and TFH cells and for the eradication of B cell derived malignancies. There is no associated input.

2016-08-01 | GSE84974 | GEO

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