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Cish attenuates homeostatic cytokine signaling to promote lung-specific macrophage programming and function

ABSTRACT: Cish attenuates homeostatic cytokine signaling to promote lung-specific macrophage programming and function

PROVIDER: PRJNA659673 | ENA |

REPOSITORIES: ENA

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Cish attenuates homeostatic cytokine signaling to promote lung-specific macrophage programming and function

Project description:Lung-specific expression of the SOCS family member Cish is driven by steady-state GM-CSF signaling and shapes alveolar macrophage identity and homeostatic function.

2021-08-26 | GSE156967 | GEO

Cish inhibits CD8+ T cell immunity and disrupts proximal T cell receptor signaling

Project description:T cell receptor (TCR) signaling is a critical process in immunity to infectious disease and cancer. Recently, a genome-wide association study has implicated polymorphisms in the CISH locus with susceptibility to infectious diseases. However, the role of Cish in the immune responses and its molecular underpinnings remains unclear. Here we demonstrate that Cish deletion resulted in protection against viral infection and enhanced CD8+ T cell tumor immunity. Transcriptome profiling revealed a hyper-TCR activation signature in Cish-deficient CD8+ T cells. Subsequent analysis revealed an inhibitory role for Cish in PLCγ1 activation, ensuing Ca2+ release and downstream signaling. In the steady-state Cish was found to physically interact with PLCγ1, however, PLCγ1 was only found to be ubiquitinated after acute TCR stimulation in the presence of Cish. These data implicate Cish as a potent negative regulator of TCR signaling and T cell immunity to infection and cancer and may have significant clinical applications. 4 biological replicates from wild-type mice and 3 biological replicates from Cish knock-out (-/-) mice were analyzed.

2015-04-30 | E-GEOD-56328 | biostudies-arrayexpress

Cish inhibits CD8+ T cell immunity and disrupts proximal T cell receptor signaling

2015-04-30 | GSE56328 | GEO

Quantitative Analysis of Wild Type and CISH-/- induced pluripotent stem cell derived NK cells (iPSC-NK) Transcriptomes

Project description:We developed human CISH-knockout (CISH-/-) NK cells using an induced pluripotent stem cell-derived NK cell (iPSC-NK cell) platform. And compare transcriptomes of CISH-/- iPSC NK cells with wild type iPSC NK cells using RNA seq. RNA seq data suggested that genes involved in the JAK-STAT signaling pathway and lymphocyte activations were significantly activated in CISH-/- iPSC NK cells.

2020-05-09 | GSE150155 | GEO

Psidium guajava cultivar:CISH-G5

Project description:Psidium guajava cultivar:CISH-G5 Raw sequence reads

| PRJNA479714 | ENA

Pro-inflammatory cytokine blockade attenuates myeloid expansion in a murine model of rheumatoid arthritis

Project description:Pro-inflammatory cytokine blockade attenuates myeloid expansion in a murine model of rheumatoid arthritis

| PRJNA531613 | ENA

Mangifera indica isolate:CISH BlockII | cultivar:Amrapali

Project description:Mangifera indica isolate:CISH BlockII | cultivar:Amrapali Transcriptome or Gene expression

| PRJNA313340 | ENA

protein turnover during homeostatic plasticity

Project description:Using quantitative proteomics we identified group of synaptic genes with decreased protein synthesis during homeostatic plasticity. To obtain further information about their mRNA levels/sequences (3’UTR) we performed polyA RNAseq. Using EISA analysis of Ribominus RNAseq dataset we could further differentiate between transcriptional respective post-transcriptional dependent alterations in mRNA levels. In addition Ribominus RNAseq from cell body and processes (dendrites, axons) RNA samples showed us local changes in mRNA levels during homeostatic plasticity. At the end, small RNAseq helped us to identify miRNAs that are increased during homeostatic plasticity and might regulate downregulated genes.

2017-04-05 | PXD004150 | Pride

CIS is a potent checkpoint in NK cell-mediated tumour immunity

Project description:Natural killer (NK) cells have evolved to detect and kill aberrant cells with this activity being governed by the cytokine interleukin (IL)-15 and foreign and self-ligands. We have identified CIS (Cytokine-inducible SH2-containing protein; Cish gene) as the critical negative regulator of IL-15 signalling in NK cells. Cish was rapidly induced in response to IL-15 and deletion of Cish rendered NK cells hypersensitive to IL-15, as evidenced by superior proliferation, survival, IFN-γ production and cytotoxicity towards tumours. This was associated with enhanced JAK/STAT signalling in Cish-deleted NK cells. Correspondingly, CIS interacted with the tyrosine kinase JAK1, inhibiting its enzymatic activity and targeting JAK for proteasomal degradation. Cish-/- mice were resistant to melanoma, prostate and breast cancer metastasis in vivo, and this was intrinsic to NK cell activity. This study has uncovered a potent checkpoint in NK cell-mediated tumour immunity and holds promise for novel immunotherapies directed at blocking CIS function.

2016-05-20 | GSE79409 | GEO

NPTX2, Homeostatic Scaling, and Schizophrenia

Project description:NPTX2, Homeostatic Scaling, and Schizophrenia

| PRJNA633132 | ENA