PD-L1 AND ICOSL DISCRIMINATE HUMAN SECRETORY AND HELPER DENDRITIC CELLS IN CANCER, ALLERGY AND AUTOIMMUNITY
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA716347 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14038033_1.fastq.gz | Fastqsanger.gz | |||
| SRR14038033_2.fastq.gz | Fastqsanger.gz | |||
| SRR14038034_1.fastq.gz | Fastqsanger.gz | |||
| SRR14038034_2.fastq.gz | Fastqsanger.gz | |||
| SRR14038035_1.fastq.gz | Fastqsanger.gz |
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Project description:PD-L1 AND ICOSL DISCRIMINATE HUMAN SECRETORY AND HELPER DENDRITIC CELLS IN CANCER, ALLERGY AND AUTOIMMUNITY [CITE-seq]
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Project description:In this study, we define a novel phenotypic and functional dichotomy of human dendritic cells (DC), with strong relevance to cancer, allergy, and autoimmunity. Using 16 different stimuli in vitro (130 observations), we describe two states of human activated DC. PD-L1highICOSLlow Secretory DC produced large amounts of inflammatory cytokines and chemokines but induced very low levels of T helper (Th) cytokines following DC-T co-culture; conversely PD-L1lowICOSLhigh Helper DC produced low levels of secreted factors but induced high levels and a broad range of Th cytokines. Secretory DC were aligned with mature migratory LAMP3+ DC in three different cancer types, atopic dermatitis, and lupus nephritis by single-cell transcriptomics. They were associated with T cell inflammation, overexpressed stimulatory and inhibitory checkpoints, acquired increased cell-cell communication, and were associated with good prognosis in head and neck squamous cell carcinoma, and with response to checkpoint blockade in Melanoma. This functional dichotomy of DC has broad implications in inflammation and immunotherapy.
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Project description:In this study, we define a novel phenotypic and functional dichotomy of human dendritic cells (DC), with strong relevance to cancer, allergy, and autoimmunity. Using 16 different stimuli in vitro (130 observations), we describe two states of human activated DC. PD-L1highICOSLlow Secretory DC produced large amounts of inflammatory cytokines and chemokines but induced very low levels of T helper (Th) cytokines following DC-T co-culture; conversely PD-L1lowICOSLhigh Helper DC produced low levels of secreted factors but induced high levels and a broad range of Th cytokines. Secretory DC were aligned with mature migratory LAMP3+ DC in three different cancer types, atopic dermatitis, and lupus nephritis by single-cell transcriptomics. They were associated with T cell inflammation, overexpressed stimulatory and inhibitory checkpoints, acquired increased cell-cell communication, and were associated with good prognosis in head and neck squamous cell carcinoma, and with response to checkpoint blockade in Melanoma. This functional dichotomy of DC has broad implications in inflammation and immunotherapy.
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Project description:The mechanisms by which regulatory T (Treg) cells differentially control allergic and autoimmune responses remain unclear. We show that Treg cells in food allergy (FA) have decreased expression of transforming growth factor beta 1 (TGF-b1) due to IL-4 and STAT6-dependent inhibition of Tgfb1 transcription. These changes were modelled by Treg cell-specific Tgfb1 monoallelic inactivation, which induced allergic dysregulation by impairing microbiota-dependent ROR-gt+ Treg cell differentiation. This dysregulation was rescued by treatment with Clostridiales species, which upregulated Tgfb1 expression in Treg cells. Biallelic deficiency precipitated fatal autoimmunity, with intense autoantibody production and dysregulated T follicular helper and B cell responses. These results identify a privileged role for Treg cell-derived TGF-b1 in regulating allergy and autoimmunity at distinct checkpoints in a Tgfb1 gene dose and microbiota-dependent manner.
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Project description:Inducible co-stimulator (ICOS) interaction with its ligand (ICOSL) is involved in several T cell effector functions. While blockade of ICOS:ICOSL interaction in chronic graft versus host disease (GVHD) seems benefi cial, results for acute GVHD remain controversial. To further elucidate its role in acute GVHD, C57BL / 6 mice were lethally irradiated and reconstituted with allogeneic spleen cells in the absence or presence of ICOSL-blocking mAb. Mice reconstituted with allogeneic spleen cells experienced severe GVHD and died untreated within 6 M-bM-^@M-^S 9 days after transplantation. Mice treated with an anti-ICOSL mAb starting from day 3 after transplantation gained weight again and survived for at least additional 12 days, although the treatment was already stopped at day 11 after transplantation. In contrast, the anti-ICOSL treatment starting from day 0 did not prevent GVHD. The diff erence between therapeutic (day 3) and prophylactic (day 0) anti-ICOSL treatment was independent of CD25 + CD4 + regulatory T cells since their depletion did not abrogate the therapeutic eff ect of ICOSL blockade. Microarray analysis revealed IFN- M-NM-3 and chemokine up-regulation in spleen cells of prophylactically treated mice, emphasizing kinetic dependence of acute GVHD modulation via blockade of ICOS:ICOSL interaction. B6 recipients were irradiated with 10.0 Gray, administered from a 137 Cs source. Splenocytes from C3H mice were prepared as single cell suspensions in PBS, depleted of red blood cells and counted. 2 M-bM-^@M-^S 3 M-CM-^W 10^7 C3H splenocytes in a volume of 200 M-NM-<l were transplanted into B6 recipients via tail vein injection (4 mice per group per experiment) 4 M-bM-^@M-^S 6 h after irradiation. Mice in the treatment group with anti-ICOSL mAb and their respective controls, received 500 M-NM-<g mAb i. p starting at day 0 or day 3, followed by subsequent injections of 200 M-NM-<g of mAb every other day. At day 4 after transplantation RNA of spleen cells was prepared and subjected to microarray analysis. Combined RNA from allogeneic transplanted mice was hybridized onto 2 independent arrays.
2009-09-14 | E-GEOD-17995 | biostudies-arrayexpress
Project description:Inducible co-stimulator (ICOS) interaction with its ligand (ICOSL) is involved in several T cell effector functions. While blockade of ICOS:ICOSL interaction in chronic graft versus host disease (GVHD) seems benefi cial, results for acute GVHD remain controversial. To further elucidate its role in acute GVHD, C57BL / 6 mice were lethally irradiated and reconstituted with allogeneic spleen cells in the absence or presence of ICOSL-blocking mAb. Mice reconstituted with allogeneic spleen cells experienced severe GVHD and died untreated within 6 – 9 days after transplantation. Mice treated with an anti-ICOSL mAb starting from day 3 after transplantation gained weight again and survived for at least additional 12 days, although the treatment was already stopped at day 11 after transplantation. In contrast, the anti-ICOSL treatment starting from day 0 did not prevent GVHD. The diff erence between therapeutic (day 3) and prophylactic (day 0) anti-ICOSL treatment was independent of CD25 + CD4 + regulatory T cells since their depletion did not abrogate the therapeutic eff ect of ICOSL blockade. Microarray analysis revealed IFN- γ and chemokine up-regulation in spleen cells of prophylactically treated mice, emphasizing kinetic dependence of acute GVHD modulation via blockade of ICOS:ICOSL interaction.
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Project description:Treg Cell TGF-β1 Regulates Distinct Checkpoints Governing Allergy and Autoimmunity
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Project description:To explore the potential function of CD19+ICOSL- B-cell-subset, the whole transcriptome of sorted CD19+ICOSL+ and CD19+ICOSL- B cells was profiled by using Microarray analysis.
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Project description:A20 is a ubiquitin-modifying protein that negatively regulates canonical NF-κB signaling and mutations in A20/TNFAIP3 have been associated with a variety of autoimmune diseases, including multiple sclerosis (MS). We found that deletion of A20 in central nervous system (CNS) endothelial cells (BEC) enhances experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. These mice showed increased numbers of CNS-infiltrating immune cells during neuroinflammation and in the steady state. While the integrity of the barrier was not impaired, we observed a strong activation of the endothelium in A20ΔBEC mice, with dramatically increased levels of the adhesion molecules ICAM-1 and VCAM-1. We furthermore discovered ICOSL as novel adhesion molecule expressed by A20-deficient BECs. Silencing of ICOSL in BECs ameliorated the severity of an active EAE disease in wildtype mice and significantly delayed the onset of symptom development. Furthermore, blocking of ICOSL on primary CNS-derived endothelial cells impaired the adhesion of different T cell populations to the monolayer. Taken together, we here report a novel function of A20-regulated ICOSL expressed on CNS endothelial cells during inflammation. We propose that BEC-ICOSL contributes to the firm adhesion of T cells to the barrier, promoting T cell transmigration into the CNS and eventually driving autoimmune neuroinflammation.
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