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Divergent role for STAT5 in the adaptive responses of natural killer cells

UID: 10805

Author(s): Lau, Colleen M.*, Sun, Joseph C.* * MSK affiliated

Description
Summary from the GEO: "Natural killer (NK) cells are innate lymphocytes with the capacity to elicit adaptive features, including clonal expansion and immunological memory. Because signal transducer and activator of transcription 5 (STAT5) is essential for NK cell development, the role of this transcription factor and its upstream cytokines IL-2 and IL-15 during infection have not been carefully investigated. In this study, we investigate how STAT5 regulates transcription during viral infection. We demonstrate that STAT5 is induced in NK cells by IL-12 and STAT4 early after infection, and that partial STAT5 deficiency results in a defective capacity of NK cells to generate long-lived memory cells. Furthermore, we find a functional dichotomy of IL-2 and IL-15 signaling outputs during viral infection, whereby both cytokines drive clonal expansion, but only IL-15 is required for memory NK cell survival. We thus highlight a novel role for STAT5 signaling in promoting an optimal antiviral NK cell response."

Overall design from the GEO: "RNA-seq was performed on Ly49H+ NK cells harvested during in vivo MCMV infection."
Subject of Study
Subject(s)
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Plain text files of expression profiling by high throughput sequencing
Accession #: GSE142821

Access via SRA

RNA sequencing of 12 samples.
Accession #: SRP239264

Access via BioProject

Additional information about the overall inititative.
Accession #: PRJNA598546

Access Restrictions
Free to All
Access Instructions
The NCBI Gene Expression Omnibus, SRA, and BioProject databases provide open access to these files. The SRA Run Selector link at the bottom of the page is a processing tool for raw data.
Associated Publications
Data Type
Equipment Used
Illumina HiSeq 4000
Software Used
SRA Toolkit
Dataset Format(s)
Plain Text
Data Tool(s)
RNA Seq
Dataset Size
830 KB (Plain text), 16.7 Gb (SRA)
Data Catalog Record Updated
2023-12-07