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Interleukin-27 signaling serves as an immunological checkpoint for innate cytotoxic cells to promote hepatocellular carcinoma

ABSTRACT: Interleukin-27 signaling serves as an immunological checkpoint for innate cytotoxic cells to promote hepatocellular carcinoma

PROVIDER: PRJNA822782 | ENA |

REPOSITORIES: ENA

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Interleukin-27 signaling serves as an immunological checkpoint for innate cytotoxic cells to promote hepatocellular carcinoma

Project description:While some of the inflammatory mechanisms driving hepatocellular carcinoma (HCC) had been proposed, the regulators of anti-cancer immunity in HCC remain poorly understood. We found that IL-27 receptor (IL-27R) signaling promotes HCC development in vivo. High IL-27EBI3 or IL-27RA expression correlated with poor prognosis for patients with HCC. Loss of IL-27R suppressed HCC in vivo in two different models of hepatocarcinogenesis. Mechanistically, IL-27R signaling within the tumor microenvironment restrains the cytotoxicity of innate cytotoxic lymphocytes. IL-27R ablation enhanced the accumulation and activation, while depletion or functional impairment of innate cytotoxic cells abrogated the effect of IL-27R disruption. Pharmacological neutralization of IL-27 signaling increased infiltration of innate cytotoxic lymphocytes with upregulated cytotoxic molecules and reduced HCC development. Our data reveal an unexpected role of IL-27R signaling as an immunological checkpoint regulating innate cytotoxic lymphocytes and promoting HCC of different etiologies, thus indicating a therapeutic potential for IL-27 pathway blockade in HCC

2022-05-27 | GSE200040 | GEO

Amyotrophic Lateral Sclerosis Transcriptomics Reveals Immunological Effects of Low-Dose Interleukin-2.

Project description:Amyotrophic Lateral Sclerosis Transcriptomics Reveals Immunological Effects of Low-Dose Interleukin-2.

| PRJNA686773 | ENA

Immunological Proteome Resource (ImmPRes): Hypoxia dataset

Project description:Third dataset release from the Immunological Proteome Resource (ImmPRes). This dataset contains the study focussing on the effect of Hypoxia in Cytotoxic CD8+ Lymphocytes.

2021-11-03 | PXD020041 | Pride

Interleukin-2 shapes the cytotoxic T cell proteome and immune-environment sensing

Project description:Interleukin-2 (IL-2) and Janus kinases (JAKs) regulate transcriptional programs and protein synthesis to control the differentiation of effector CD8+ cytotoxic T cells (CTL). Using high-resolution mass spectrometry, we have generated an in-depth characterisation of how IL-2 and JAKs configure the CTL proteome to control CTL function. We found that IL-2-JAK1/3 signaling selectively regulated the abundance of a key subset of proteins influencing the accumulation of critical cytokines and effector molecules in T cells. Moreover, IL-2 controlled the concentration of proteins that support core metabolic processes essential for cellular fitness. One fundamental insight was the dominant role for IL-2 in controlling how effector T cells respond to their microenvironment. IL-2-JAK1/3 signaling pathways thus controlled the abundance of nutrient transporters, nutrient sensors and critical oxygen sensing molecules. The data provide key insights of how IL-2 controls T cell function and highlight signaling mechanisms and transcription factors that link oxygen sensing to transcriptional control of CD8+ T cell differentiation.

2018-04-17 | PXD008112 | Pride

Interleukin 21 drives CXCR6+ CD8+ T cell mediators in Autoimmune Checkpoint Inhibitor Thyroiditis

Project description:Checkpoint inhibitor (ICI) immunotherapy leverages the body’s own immune system to attack cancer cells but leads to unwanted autoimmune side effects in up to 60% of patients. Such immune related adverse events (IrAE) lead to treatment interruption, permanent organ dysfunction, hospitalization and premature death. Thyroiditis is one of the most common IrAE, but the cause of thyroid IrAE remains unknown. To delineate human IRAE pathogenesis, we sampled thyroid tissue from subjects with ICI-thyroiditis and HT. Using single cell RNA sequencing of human thyroid fine needle aspiration (FNA) specimens, we identify CXCR6+ interferon gamma (IFN)+ cytotoxic CD8+ T cells as key contributors to ICI-thyroiditis (IRAE). This is in contrast to the primary role for CD4+ Th17 cells in the pathogenesis of HT (14, 15). Interestingly, we also found a supporting role for IL21-producing CD4+ T follicular (Tfh) and peripheral helper (Tph) cells via the upregulation of CXCR6 and cytotoxic function in CD8+ T cells.

2023-05-17 | GSE218743 | GEO

Immunological Proteome Resource (ImmPRes): Part two

Project description:Second dataset release from the Immunological Proteome Resource (ImmPRes). This dataset contains both lymphoid and myeloid populations. The whole list is as follows: Bone marrow derived eosinophils, bone marrow derived mast cells, bone marrow derived macrophages, NK cells, TH2 cells, TH17 cells, Cytotoxic T cells cultured in IL15 and Naive CD8+ T cells extractred from the lymph nodes of C57BL/6J mice.

2020-07-02 | PXD020091 | Pride

Interleukin-18 and cytotoxic impairment are independent and synergistic causes virus-induced hyperinflammation in mice

Project description:Interleukin-18 and cytotoxic impairment are independent and synergistic causes virus-induced hyperinflammation in mice

| PRJNA631034 | ENA

Cytotoxic Innate Lymphoid Cells Sense Cancer Cell-Expressed Interleukin-15 to Suppress Human and Murine Malignancies

Project description:Cytotoxic Innate Lymphoid Cells Sense Cancer Cell-Expressed Interleukin-15 to Suppress Human and Murine Malignancies

| PRJNA821509 | ENA

Clonally expanded CD38hi cytotoxic CD8 T cells define the T cell infiltrate in checkpoint inhibitor-associated arthritis

Project description:Immune checkpoint inhibitor (ICI) therapies have improved outcomes for advanced malignancies by activating T cell responses, yet often also elicit harmful autoimmune reactions. The T cell mechanisms mediating these iatrogenic autoimmune events remain unclear. Here we focused on ICI-induced inflammatory arthritis (ICI-arthritis), which can clinically present indistinguishable from rheumatoid arthritis (RA). Compared to autoimmune RA and psoriatic arthritis (PsA), we found ICI-arthritis joints contained an expanded CD38hiCD127- CD8 T cell subset that displays cytotoxic, effector, and interferon (IFN) response signatures. Synovial T cells exposed to Type I IFN, more so than IFN-γ, induced the CD38hi cytotoxic phenotype. Single cell transcriptomic and T cell repertoire (TCR) analyses indicated the abundant CD38hi CD8 T cells resulted from local proliferation of a limited number of clones. The CD38hi phenotype was distinct from dysfunctional T cells and clonally most related to a TCF7+ memory population. Comparing CD8 T cells from both knees in a patient demonstrated considerable sharing of the CD38hi expanded TCR clonotypes. Further, expanded TCR clonotypes from the joints were detected in the circulation, and together with higher frequencies of circulating CD38hi CD8 T cells, represent potential biomarkers for irAEs. These results define a distinct CD8 T cell subset in humans that is activated by ICI therapy and mediates tissue-specific autoimmunity.

2023-12-31 | GSE205501 | GEO

In-depth analysis of the phosphoprotein landscape of cytotoxic T lymphocytes and its regulation by cytokines

Project description:Here we present high-resolution mass spectrometry analysis of changes to the phosphoproteome of cytotoxic T lymphocytes (CTL) induced by the cytokine, Interleukin 12 (IL-12). We treated CTL with a short and long IL-12 stimulation and mapped the changes to the phosphoproteome using quantitative SILAC-based phosphoproteomics.

2016-08-24 | PXD004644 | Pride

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