Transcriptional analysis of Wt and CXCR5-KO cDC subsets
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE301250 | GEO | 2025/11/14
REPOSITORIES: GEO
Similar Datasets
Project description:Mouse bone marrow derived macrophages were stimulated with L3 larvae of the helminth Heligmosomoides polygyrus (Hp) (500 L3 /1 mio cells) in the presence or absence of immune serum (1:50 v:v) from challenge-Hp-infected mice.
2013-12-31 | E-MEXP-3920 | biostudies-arrayexpress
Project description:Transcriptional analysis of Wt and CXCR5-KO cDC subsets
| PRJNA1284336 | ENA
Project description:This study used single cell RNA sequencing of small intestinal ILC2s +60 days after helminth infection (Nippostrongylus brasiliensis-Nb. or Heligmosomoides polygyrus, Hp.) and in age matched naïve mice (Ctrl) to study memory ILC2 gene signatures after helminth infection.
2025-07-28 | GSE301975 | GEO
Project description:In chronic infections, sustaining the CD4 T cell responses is crucial for pathogen clearance. The expression of inhibitory receptors such as LAG-3 or Lymphocyte activation gene 3 is usually associated with immune suppression and T cell exhaustion. However, LAG-3 also serves as an immune checkpoint molecule and is implicated in proliferation control and cell survival. In this study, we have utilized a mouse model of visceral leishmaniasis (VL), to characterize a subset of LAG-3- and CXCR5-expressing CD4 T cells. These LAG-3+CXCR5+PD-1lo/int CD4 T cells exist in naïve mice, they expand during VL, and are antigen specific. Importantly, the RNAseq analysis showed that these cells highly express gene signatures associated with self-renewal capacity, indicating that these cells might act as progenitors. Additionally, upon adoptive transfer into Rag1-/- mice followed by challenge with Leishmania donovani, these LAG-3+CXCR5+ PD-1lo/int CD4 T cells gave rise to different types of T effector and regulatory subsets, demonstrating their differentiation potential. These cells were also observed in mice infected with LCMV clone-13 and Heligmosomoides polygyrus bakeri. In summary, we propose that these LAG-3+CXCR5+ PD-1lo/int CD4 T cells that exhibit progenitor-like capacities could be implicated in maintaining CD4 T cell responses in chronic infections.
2024-02-13 | GSE255333 | GEO
Project description:Four microRNAs(miRNAs) highly abundantly secreted by the parasitic nematode Heligmosomoides polygyrus were synthesized (miRVana, Ambion) and transfected repeatedly into differentiating Th2 cells in vitro, individually or in combination. The effects of the different transfection regimens were assessed by RNA sequencing (Illumina).
2022-06-07 | GSE180829 | GEO
Project description:Gene expression of Treg cells that have lost Foxp3 expression and acquired Il4 expression following adoptive transfer into T-cell deficient mice (HpTR-IL-4gfp+), cmpared to conventional Treg cells isolated from H. polygyrus-infected wild-type mice (HpTR) and Th2 cells generated from naïve T cells following adoptive transfer into H. polygyrus-infected T-cell deficient mice (nT-IL-4gfp+). Immunity to intestinal helminth infections requires the rapid activation of T helper 2 (Th2) cells. However, simultaneous expansion of regulatory CD4+Foxp3+ T (Treg) cells impedes protective responses, resulting in chronic infections. The ratio between regulatory and effector T cells can therefore determine the outcome of infection. The re-differentiation of Treg into T helper (Th) cells has been identified in hyper-inflammatory diseases. In this study, we asked whether ex-Treg Th2 cells develop and contribute to type 2 immunity. Using multi-gene reporter and fate-reporter systems we demonstrate that a significant proportion of Th2 cells derive from Foxp3+ cells following Heligmosomoides polygyrus infection and airway allergy. Ex-Foxp3 Th2 cells exhibit characteristic Th2 effector functions and provide immunity to H. polygyrus. Through selective deletion of Il4ra on Foxp3+ cells, we further demonstrate IL-4 is required for the development of ex-Foxp3 Th2 cells. Collectively, our findings indicate that converting Treg cells into Th2 cells could concomitantly enhance Th2 cells and limit Treg-mediated suppression.
2017-05-04 | GSE98518 | GEO
Project description:CD8+ T-cells inhibit virus replication in SIV-infected rhesus macaques (RM). However, it is not clear how SIV infection is controlled in germinal center during chronic SIV infection and limited information exists on the characteristics of CXCR5+ CD8 T cells during chronic SIV/HIV infection. In this study, we used functional genomics to investigate characteristic features and potential mechanisms of CXCR5+ and CXCR5- SIV specific CD8 T cells for the control of pathogenic SIV infection. Six chronically SIV infected RMs, three SIVE660 infected and three SIV mac251 infected that are positive for Mamu A01 allele were selected and SIV-specific CXCR5+ and CXCR5- CD8 T cells were sorted based on CXCR5 expression. RNA from sorted cells were extracted and microarray were performed and analysed. Principal component analysis demonstrated that overall gene expression difference between CXCR5+ and CXCR5- SIV-specific CD8 T cells. Interestingly, the CXCR5+ CD8 T cells revealed a distinct gene signature pattern when compared to CXCR5- CD8 T cells. Unlike the CXCR5- CD8 T cells, the CXCR5+ CD8 T cells expressed higher levels of genes associated with Tfh CD4 T cells such as the master transcription factor Bcl6, CD200, and CTLA4 as well as markers associated with Th2 CD4 T cells such as IL-4R (CD124), CCR4, STAT6, NFATC, and IL-10. Effector molecules typically observed in cytotoxic CD8 T cells such as granzyme A, B, and K were expressed at lower levels on CXCR5+ CD8 T cells compared to their CXCR5- counterparts. CXCR5+ CD8 T cells also expressed higher levels of molecules associated with co-stimulation/antigen presentation such as CD40, CD83, 41BBL and MAMU-DRA. The CXCR5+ CD8 also expressed higher levels of inhibitory receptors such as CD200 and SPRY2 but lower levels of other inhibitory receptors CD160 and CD244. The functional consequence of the expression of these molecules is yet to be determined. Additionally, CXCR5+ CD8 T cells expressed higher levels of the anti-apoptotic gene Bcl-2 and lower levels of the pro-apoptotic gene annexin, suggestive of their better survival potential during chronic SIV infection. Collectively, these results demonstrate that SIV specific CXCR5+ CD8 T cells possess a unique gene expression signature compared to SIV-specific CXCR5- CD8 T cells.
2017-03-07 | GSE74751 | GEO
Project description:Bcl6/Blimp1 are well-known for Tfh cell determination, but they are dispensable in regulating the expression of CXCR5, which is critical for Tfh migration into germinal center (GC). In this study, we uncovered a novel pair of transcription factors, Bhlhe40/Pou2af1, that regulate Tfh maturation through regulation of CXCR5. Pou2af1 promotes Tfh generation by upregulating CXCR5, while Bhlhe40 represses Tfh differentiation by inhibiting Pou2af1. Pou2af1 was further verified being essential for GC Tfh cell localization, whereas Bhlhe40 inhibits pre-Tfh cells import into GC. Such migration behavior change can be explained by an alteration in the MFI of CXCR5. RNA-Seq analysis confirmed Bhlhe40 inhibiting Pou2af1 and the requirement of Pou2af1 upregulation in optimal CXCR5 expression. Thus, our study filled a long-standing gap in the regulation of optimal CXCR5 expression by revealing a key transcriptional regulatory circuit involving Bhlhe40/Pou2af1, which operates downstream of the Bcl6/Blimp-1 circuit that determines Tfh cell fate. RNA-Seq analysis of gene expression in T cell subsets (Th1, Th2, Th17 and iTreg), which are primed and differentiated in vitro from WT mice or Bhlhe40f/f-CD4Cre mice. RNA-Seq analysis of gene expression in antigen-specific Tfh cells and non-Tfh cells, which were sorted from the indicated bone marrow chimera mice (WT, Pou2af1-/-, Bhlhe40-/-). ChIP-Seq analysis of binding sites by Bhlhe40 in Th1, Th2, Th17 and iTreg. ChIP-Seq analysis of binding sites by Pou2af1 in splenic B cells.
2025-09-21 | GSE247137 | GEO