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Gene expression profile of CD4+ T-cells restimulated by anti-CD3 and anti-ICOS compared to anti-CD3 alone

ABSTRACT: Engagement of the ICOS receptor represents a key event in a process that culminates in Bcl6 expression and acquisition of the TFH and TFR phenotype. To better understand the essentials of ICOS-mediated signaling pathway, we profiled the changes in gene expression elicited after co-ligation of ICOS and CD3 compared with CD3 ligation alone.

ORGANISM(S): Mus musculus

PROVIDER: GSE61284 | GEO | 2014/09/23

SECONDARY ACCESSION(S): PRJNA260647

REPOSITORIES: GEO

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Gene expression profile of CD4+ T-cells restimulated by anti-CD3 and anti-ICOS compared to anti-CD3 alone

Project description:Engagement of the ICOS receptor represents a key event in a process that culminates in Bcl6 expression and acquisition of the TFH and TFR phenotype. To better understand the essentials of ICOS-mediated signaling pathway, we profiled the changes in gene expression elicited after co-ligation of ICOS and CD3 compared with CD3 ligation alone. Naïve CD4+ T-cells were purified from single cell suspensions of B6 spleen and stimulated with anti-CD3 and anti-CD28 for 2d followed by resting overnight before 20 min of incubation with anti-CD3 and/or anti-ICOS and cross-linking with goat anti-hamster Ab for 8h. RNA was prepared, amplified, labeled and hybridized to Mouse Gene 1.0 ST Array (Affymetrix), in quadruplicates for anti-CD3 ligation and duplicates for anti-CD3/ anti-ICOS co-ligation.

2014-09-23 | E-GEOD-61284 | biostudies-arrayexpress

ICOS costimulation is indispensable for the differentiation of T follicular regulatory cells

Project description:ICOS is a T cell costimulatory receptor critical for Tfh cell generation and function. However, the role of ICOS in Tfr cell differentiation remains unclear. Using Foxp3-Cre-mediated ICOS knockout (ICOS FC) mice, we show that ICOS deficiency in Treg-lineage cells drastically reduces the number of Tfr cells during GC reactions but has a minimal impact on conventional Treg cells. Single-cell transcriptome analysis of Foxp3+ cells at an early stage of the GC reaction suggests that ICOS normally inhibits Klf2 expression to promote follicular features including Bcl6 upregulation. Further, ICOS costimulation promotes nuclear localization of NFAT2, a known driver of CXCR5 expression. Notably, ICOS FC mice had an unaltered overall GC B cell output but showed signs of expanded autoreactive B cells along with elevated autoantibody titers. Thus, our study demonstrates that ICOS costimulation is critical for Tfr cell differentiation and highlights the importance of Tfr cells in maintaining humoral immune tolerance during GC reactions.

2023-02-02 | GSE164995 | GEO

RNA-seq of purified T cells treated with KY1044 + anti-CD3 against anti-CD3 treated controls

Project description:KY1044 is a human monoclonal IgG1 that selectively binds to Inducible T cell CO-stimulator (ICOS). The co-stimulatory effect of KY1044-stimulated human T cells was analysed by RNA sequencing (RNA seq). Purified pre-activated (ICOS+ve) T cells were stimulated with either KY1044 and anti-CD3 or anti-CD3 alone and cells were harvested for RNA seq after 6hrs. Kallisto transcript abundance are provided in the absence of raw sequence reads.

2020-09-01 | E-MTAB-9500 | biostudies-arrayexpress

Impaired T-cell function in patients with novel ICOS

Project description:Interaction of ICOS - ICOS ligand is required for the germinal center formation, T-cell immune responses, and development of autoimmune diseases. Human ICOS deficiency with the identical ICOS mutation has been identified in nine patients worldwide. In vitro studies showed T-cell defect of the patients was mild, and in vivo autoimmunity was uncommon and mild. Here we report in-depth analysis of T-cell function in two siblings with novel ICOS deficiency. While the brother displayed mild skin infections, psoriasis-like skin region, and defective immunoglobulin class switching, the sister had more severe symptoms, which included immunodeficiency, rheumatoid arthritis, inflammatory bowel disease, interstitial pneumonitis, and psoriasis. Despite of normal CD3/CD28-induced proliferation and IL-2 production in vitro, peripheral blood T-cells from both patients demonstrated decreased percentage of CD4 central and effector memory T-cells and impaired production of Th1, Th2, and Th17 cytokines upon CD3/CD28 costimulation or upon PMA/ionophore stimulation. The defective polarization into effector cells were associated with impaired induction of T-bet, GATA3 and MAF and RORC. Reduced CTLA-4+CD45RO+ FoxP3+ regulatory T-cells and diminished induction of inhibitory cell surface molecules including CTLA-4 were also observed in the patients. Further analysis of the gene expression and immune functions of the patients demonstrated increased induction of RANKL, lack of IFN-g response, and loss of Itch expression upon activation in the female case with autoimmunity. Our study suggests extensive T-cell dysfunction and loss of balance between effector cells and regulatory cells in the ICOS-deficient patients may account for their immunodeficiency and/or autoimmune disorder.

2008-09-26 | GSE12875 | GEO

ICOS-expressing Treg cells influence the composition of anti-tumor CTL population

Project description:The role of ICOS in anti-tumor T cell responses and overall tumor progression has been controversial. Here, we compared tumor progression in mice lacking ICOS only in Treg cells or in all T cells. We found that Treg-specific ICOS knockout reduces the overall tumor burden compared to Cre control mice with increased T effector/Treg ratios in the tumor. In contrast, there was no difference in the tumor burden in mice lacking ICOS in all the T cell compartments. This suggests a dual role of ICOS costimulation in promoting pro- and anti-tumor T cell responses. Consistent with reduced tumor burden, we found that Treg-specific deletion of ICOS leads to an increase of CD8+ CTLs that express high levels of granzyme B and perforin. Moreover, single-cell transcriptome analysis revealed an increase of Ly108hiEomeshi CD8+ T cell subset at the cost of Ly108hiT-bethi subset in Treg-specific knockout mice. These results suggest that ICOS-expressing Treg cells suppress CTL maturation process at the level of Eomes upregulation, a critical step known to drive perforin expression and cytotoxicity. Collectively, our data imply that cancer immunotherapies using ICOS agonist antibodies would work better in Treg-low tumors or when they are combined with regimens that deplete tumor-infiltrating Treg cells.

2024-07-18 | GSE226471 | GEO

Non-coding autoimmune risk variant accelerates T peripheral helper cell development via ICOS

Project description:Fine-mapping and functional studies implicate rs117701653, a common non-coding variant in the CD28/CTLA4/ICOS locus, as a contributor to risk for rheumatoid arthritis and type 1 diabetes. Using DNA pulldown, mass spectrometry, genome editing and eQTL analysis, we establish that the disease-associated allele reduces affinity for the inhibitory chromosomal regulator SMCHD1 to drive expression of inducible T-cell costimulator (ICOS), enhancing memory CD4+ T cell ICOS expression in individuals bearing the risk allele. Higher ICOS expression is paralleled by an increase in circulating T peripheral helper (Tph) cells, and in rheumatoid arthritis patients, of blood and joint fluid Tph cells and circulating plasmablasts, suggesting a causal link. Indeed, ICOS ligation accelerates T cell differentiation into CXCR5-PD-1high Tph cells producing IL-21 and CXCL13, as does carriage of the rs117701653 risk allele. Thus, mechanistic dissection of a causal non-coding variant in human autoimmunity discloses a new pathway through which ICOS regulates Tph abundance.

2023-07-01 | GSE235868 | GEO

Gene expression comparison between the murine T-cell hybridoma 6-13-64 ICOS(-) population and ICOS(+) population

Project description:ICOS (Inducible Costimulator) is a T cell costimulatory molecule. We found that the cloned T-cell hybridoma 6-13-64 consists of two populations, ICOS expressing and non-expressing. The aim of this study is to screen for candidate genes that regulate ICOS gene expression by transcriptional profiling and comparison of the ICOS-positive and ICOS-negative subpopulations isolated from the 6-13-64 T-cell hybridoma. One-condition experiment, ICOS(-) vs. ICOS(+) cells. Independently grown and harvested. One replicate per array.

2012-03-31 | E-GEOD-20922 | biostudies-arrayexpress

Gene expression comparison between the murine T-cell hybridoma 6-13-64 ICOS(-) population and ICOS(+) population

2012-04-01 | GSE20922 | GEO

Proteome and (ox)PTP profile analysis of diabetic NOD mouse under single (anti-CD3) or combined (anti-CD3 + IL1RA) treatment

Project description:Type 1 diabetes (T1D) results from autoimmune destruction of β cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell function. Here, we assessed the global protein and individual PTP profile in the pancreas of diabetic NOD mice treated with anti-CD3 mAb and IL-1RA combination therapy. The treatment reversed hyperglycemia compared to the anti-CD3 alone control group. We observed enhanced expression of PTPN2, a T1D candidate gene, and endoplasmic reticulum (ER) chaperones in the islets from cured mice.

2022-11-10 | PXD025394 | Pride

scRNA-seq of human Tfh, Tfr and Treg cells sorted from Tonsil, Iliac Lymph Node and PBMCs

Project description:The datasets were obtained to investigate the transcriptional profile of Tfh, Tfr and Treg cells isolated from different human tissues. The comparison between lymphoid tissues with different frequency of the most mature Tfh and Tfr cells allows the investigation of maturation as well as tissue adaptation of those different cell subsets. To address these issues, three different cell populations from three different tissues were sorted by index sorting, with Tfh cells as CD4+CXCR5+ICOS+; Tfr cells as CD4+CXCR5+CD25+ and Treg cells as CD4+CXCR5-CD25+. Smart-seq2 protocol was used mRNA library preparations.

2021-04-22 | E-MTAB-10364 | biostudies-arrayexpress

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