Cell intrinsic changes in transcription of naïve CD4 T cells upon S1pr1 deletion
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE97249 | GEO | 2017/05/26
SECONDARY ACCESSION(S): PRJNA381079
REPOSITORIES: GEO
Similar Datasets
Project description:We compared gene expression between WT CD4+ (CD45.1) and Myd88-/- CD4+ (CD45.2) T cells from the spleen of infected mix bone marrow chimeras at day 14 of T. cruzi infection. The hypothesis studied in this experiment was that MyD88-/- CD4+ cells have suppressed Th1 differentiation potencial when compared to WT CD4+ T cells. The results indicate that CD4+ T cell-intrinsic MyD88 signaling is necessary for sustaining a more robust Th1 differentiation program and increased expansion among WT CD4+ T cells, resultant of relative higher proliferation and lower apoptosis Total RNA obtained from isolated CD4+ T cells from the spleen of infected mix bone marrow chimeras at day 14 of T. cruzi infection.
2014-08-20 | E-GEOD-57738 | biostudies-arrayexpress
Project description:Naive CD4+ T cells (CD4+CD25-CD44-CD62L+) were FACS sorted from WT or T cell conditional GOT1-/- C57BL/6 mouse spleen and lymph nodes. Sorted cells were differentiated into Th17 cells in the presence of TGFβ, IL1β, IL6, IL23, anti-IFNγ and anti-IL4. RNA sequencing was then performed on day4 differentiated TH17 cells.
2023-02-02 | GSE215115 | GEO
Project description:Nonobese diabetic (NOD) mice congenic for B10 derived genes in the Idd9 region of chromosome 4 are highly protected from the development of diabetes. In order to identify possible candidate genes within the Idd9 susceptibility region and possible downstream mediators of protection, we compared gene expression between NOD and Idd9 CD4+ T-cells. CD4+ T-cells with an activated phenotype (CD44-high/CD62L-low) were sorted from the pancreatic lymph nodes of female 8-week old mice. Mice were bred at Taconic farms and were line 905 (NOD.B10-Idd9 congenic) and line 6359 (NOD-like control strain with a B10 congenic region on chromosome 1 which does not modify diabetes incidence). Three replicate samples were prepared, each from four pooled pancreatic lymph nodes. CD4+CD44-highCD62L-low T-cells were sorted from each sample.
2012-02-01 | E-GEOD-35482 | biostudies-arrayexpress
Project description:We compared gene expression between WT CD4+ (CD45.1) and Myd88-/- CD4+ (CD45.2) T cells from the spleen of infected mix bone marrow chimeras at day 14 of T. cruzi infection. The hypothesis studied in this experiment was that MyD88-/- CD4+ cells have suppressed Th1 differentiation potencial when compared to WT CD4+ T cells. The results indicate that CD4+ T cell-intrinsic MyD88 signaling is necessary for sustaining a more robust Th1 differentiation program and increased expansion among WT CD4+ T cells, resultant of relative higher proliferation and lower apoptosis
2014-08-20 | GSE57738 | GEO
Project description:Analysis of T-cells lacking the proprotein convertase furin. Proprotein convertases promote the proteolytic maturation of proproteins. Furin is induced in activated T-cells. Results provide insight into the function of furin in T-cells. CD4+CD62L+CD44- naive, CD4+CD62L-CD44+ memory and CD4+CD25+FoxP3+ regulatory T cells were isolated from Fur flox/flox and CD4 cre Fur flox/flox mice. Naive T cells were activated via TCR. Total RNA was extracted from all cells and hybridized to Affymetrix microarrays.
2015-08-05 | E-GEOD-67884 | biostudies-arrayexpress
Project description:Innate memory phenotype (IMP) CD4+ T cells are non-conventional αβ T cells exhibiting features of innate immune cells, characterized as CD44high and CD62Llow in periphery. It is recently reported by our group that bone marrow chimeric mice lacking thymic MHCI expression develop predominantly IMP CD8+ T cells, while those lacking hematopoietic MHCI develop predominantly naïve CD8+ T cells. Here we perform hirarchical clustering analysis and found that CD4+ T cells share similar property: chimeras lacking thymic MHCII gave rise to predominantly CD4+ T cells that resemble IMP CD4+ T cells observed in WT mice, and vice versa, chimeras lacking hematopoietic MHCII had a majority of naïve-like CD4+ T cells resembling naïveCD4+ T cells seen in WT mice. We used microarrays to compare the global programme of gene expression to determine whether the hematopoietic MHCII selected CD4+ T cells are IMP, and whether the thymic MHCII selected CD4+ T cells are naïve CD4+ T cells as observed in WT mice. Through hierarchical clustering and analysis of global gene differential expression, we determined that hematopoietic MHCII dependent IMP CD4+ T cells generated from WT bone marrow transplanted into irradiated MHCII-/- recipients, resemble IMP CD4+ T cells in WT mice, while naïve CD4+ T cells generated from MHCII-/- bone marrow transplanted into irradiated WT recipients, resemble naïve CD4+ T cells in WT mice. Cell Sorting was performed using a Cytopeia Influx Cell Sorter. Chimeric IMP (CD45.1+TCRβ+CD4+CD44highCD62Llow) CD4+ T cells were sorted from splenocytes of CD45.1+WTâCD45.2+MHCII-/- chimeras (WM IMP CD4), and chimeric naïve (CD45.2+TCRβ+CD4+CD44lowCD62Lhigh) CD4+ T cells were sorted from splenocytes of CD45.2+MHCII-/- â CD45.1+WT chimeras (MW naïve CD4) respectively, 8 weeks post transplantation. WT IMP (TCRβ+CD4+CD44highCD62Llow) and naïve (TCRβ+CD4+CD44lowCD62Lhigh) CD4+ T cells were sorted from splenocytes of 8-week old WT mice.
2014-03-14 | E-GEOD-46892 | biostudies-arrayexpress
Project description:Nonobese diabetic (NOD) mice congenic for B10 derived genes in the Idd9 region of chromosome 4 are highly protected from the development of diabetes. In order to identify possible candidate genes within the Idd9 susceptibility region and possible downstream mediators of protection, we compared gene expression between NOD and Idd9 CD4+ T-cells. CD4+ T-cells with an activated phenotype (CD44-high/CD62L-low) were sorted from the pancreatic lymph nodes of female 8-week old mice.
2012-02-01 | GSE35482 | GEO
Project description:Impaired T cell immunity in the elderly increases mortality from infectious disease. The branching of Asparagine-linked glycans is a critical negative regulator of T cell immunity. We found that N-glycan branching increases with age in female > male, naïve > memory and CD4+ > CD8+ T cells, likely contributing to immunosenescence. To investigate the mechanisms driving these changes, we performed RNA-seq analysis on highly purified young and old naive (CD3+CD4+CD25-CD62L+CD44-) and effector memory (CD3+CD4+CD25-CD62L-CD44+) CD4+ T cells from male and female mice. Comparing young and old CD4+ TN cells, 158 and 192 differentially expressed genes (DEGs) were identified in females and males, respectively. Remarkably, only 44 of these overlapped between the sexes. There were no significant differences in gene expression of N-glycan branching enzymes or other relevant glycosylation genes. Among the 114 DEGs in female but not male CD4+ TN cells, four were within the IL-7 signaling pathway, a pathway previously implicated in regulating N-glycan branching. This included reduced expression of IL7Rα (CD127) and increased expression of Suppressor of cytokine signaling 1 (Socs1), Socs3, and Janus kinase 3 (Jak3). Other IL-7 signaling pathway genes were unchanged.
2022-01-14 | GSE184496 | GEO
Project description:Transcriptomic evaluation of CD4+CD62L-CD44+FoxP3-CD45RbLo (RbLo TEM) versus CD4+CD62L+CD44-FoxP-CD45RbHi (RbHi TN) cells following activation
| PRJNA350815 | ENA
Project description:Developing CD4+ T-cells in the thymus mature from CD69+Qa2- cells to CD69-Qa2+ T-cells. This maturation is accombanied by increased expression of CD62L and S1PR1 in Qa2+ cells, which allows mature T-cells to emigrate from the thymus to the periphery. However, miR-142-/- mice are characterized by an altered thymocytes homeostasis, characterized by reduced CD62L protein levels on their cell surface. To characterize the underlying molecular mechanisms, which lead to reduced CD62L expression in miR-142-/- CD4+ thymocytes, we investigated the mRNA levels in immature Qa2- as well as mature Qa2+ thymocytes isolated ex vivo from WT and miR-142 deficient Bl6 mice.
2013-06-14 | GSE47909 | GEO