Study Instance

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        "type": "studies",
        "id": "MGYS00001223",
        "attributes": {
            "bioproject": "PRJEB8991",
            "samples-count": 30,
            "accession": "MGYS00001223",
            "is-private": false,
            "last-update": "2024-06-28T16:27:23",
            "secondary-accession": "ERP010045",
            "centre-name": "MHH",
            "public-release-date": null,
            "study-abstract": "The epithelium is the major entry point for many viruses but the processes protecting barrier surfaces against viral infections are incompletely understood. We identify interleukin (IL)-22 produced by group 3 innate lymphoid cells (ILC3s) as an amplifier of interferon (IFN)-lambda signaling, a synergism required to curtail replication of rotavirus, the leading cause of childhood gastroenteritis. Cooperation between IL-22 and IFN-lambda receptors, both of which are preferentially expressed by intestinal epithelial cells, was required for optimal STAT1 transcription factor activation and expression of interferon-stimulated genes. This data suggests that epithelial cells are protected against virus replication by co-opting two evolutionarily related cytokine networks. These data may inform the design of novel immunotherapies of virus infections that are sensitive to IFNs.",
            "study-name": "Interferon-lambda and interleukin-22 cooperate for the induction of interferon-stimulated genes and control of rotavirus infection",
            "data-origination": "SUBMITTED"
        },
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                "data": []
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                    {
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                        "id": "root:Host-associated:Mammals:Digestive system:Large intestine",
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