Global transcriptional analysis delineates the differential inflammatory response interleukin-15 elicits from cultured human T cells

Ramsborg, Christopher G.; Papoutsakis, E. T.

doi:10.1016/j.exphem.2006.11.013

Cited by 22 publications

(21 citation statements)

References 71 publications

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“…IL-15 increases proliferation and immunoglobulin secretion by B cells as well as up-regulates expression of co-stimulatory molecules such as CD40L (42). In a study examining an experimental Pneumocystis vaccine in which CD40L was co-expressed, it was reported that antibodies to Pneumocystis were induced independent of CD4 + status (43).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-15 and Its Receptor Augment Dendritic Cell Vaccination against theneuOncogene through the Induction of Antibodies Partially Independent of CD4 Help

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Interleukin-15 and Its Receptor Augment Dendritic Cell Vaccination against theneuOncogene through the Induction of Antibodies Partially Independent of CD4 Help

et al. 2010

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“…Indeed, NFIL3 is induced by several cytokines and hormones, including IL-3, IL-4, IL-6, insulin, and PTH (8,9,(13)(14)(15)(16)(17)(18)(19). This suggests that NFIL3 is the critical mediator to induce cytokine-dependent cellular activation and differentiation.…”

Section: Discussionmentioning

confidence: 99%

IL-4-induced transcription factor NFIL3/E4BP4 controls IgE class switching

Kashiwada

Levy

McKeag

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

153

139

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IL-4 signaling promotes IgE class switching through STAT6 activation and the induction of Ig germ-line ε (GLε) transcription. Previously, we and others identified a transcription factor, Nfil3, as a gene induced by IL-4 stimulation in B cells. However, the precise roles of nuclear factor, IL-3-regulated (NFIL3) in IL-4 signaling are unknown. Here, we report that NFIL3 is important for IgE class switching. NFIL3-deficient mice show impaired IgE class switching, and this defect is B-cell intrinsic. The induction of GLε transcripts after LPS and IL-4 stimulation is significantly reduced in NFIL3-deficient B cells. Expression of NFIL3 in NFIL3-deficient B cells restores the impairment of IgE production, and overexpression of NFIL3 in the presence of cycloheximide induces GLε transcripts. Moreover, NFIL3 binds to Iε promoter in vivo. Together, these results identify NFIL3 as a key regulator of IL-4-induced GLε transcription in response to IL-4 and subsequent IgE class switching.IL-4 signal | immunoglobulin | germ-line transcription

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“…[62][63][64][65] Similarly, OSM expression can be induced in a STAT5-dependent fashion by other cytokines, including erythropoietin (Epo), G-CSF (granulocyte colony-stimulating factor), IL-2 and IL-3. 66-68 Additional STAT5-activating cytokines have also been shown to induce OSM expression, including GM-CSF (granulocytemacrophage colony-stimulating factor) 46,52,56,60 and IL-15, 69 although these studies did not directly confirm a role for STAT5. Notably, in response to GM-CSF or the protein kinase-C activator PMA (phorbol 12-myristate 13-acetate), neutrophils secrete considerable quantities of preformed OSM protein within minutes and continue to release newly synthesized OSM with prolonged stimulation.…”

Section: Regulation Of Osm Productionmentioning

confidence: 99%

The oncostatin M‐stromal cell axis in health and disease

West¹,

Owens

Hegazy

2018

Scand J Immunol

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The field of stromal immunology has risen to prominence in the last decade, fuelled by accumulating evidence that nonhaematopoietic mesenchymal cells are not simply involved in modulating tissue structure, but actively contribute to immune processes. In addition to regulating tissue integrity during homoeostasis, stromal cells are sensitive sensors of inflammatory stimuli produced downstream of tissue injury or infection, and respond by producing a wide variety of chemokines, cytokines and adhesion factors that contribute to immunity and tissue repair. When not appropriately regulated, these same processes can result in inflammatory pathology and organ dysfunction. In this review, we provide a brief overview of stromal immunology, followed by a comprehensive discussion of how the IL-6 family cytokine oncostatin M (OSM) coordinates stromal cell activity in diverse physiological and pathological contexts. We conclude by providing a perspective on the potential clinical value of the OSM-stromal cell axis and how this pathway might be exploited therapeutically.

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Global transcriptional analysis delineates the differential inflammatory response interleukin-15 elicits from cultured human T cells

Abstract: These findings suggest that exogenous IL-15 may have a potential role in adoptive immunotherapy by both enhancing proliferation and modulating functionality during ex vivo T-cell expansion.

Cited by 22 publications

References 71 publications

Interleukin-15 and Its Receptor Augment Dendritic Cell Vaccination against theneuOncogene through the Induction of Antibodies Partially Independent of CD4 Help

Interleukin-15 and Its Receptor Augment Dendritic Cell Vaccination against theneuOncogene through the Induction of Antibodies Partially Independent of CD4 Help

IL-4-induced transcription factor NFIL3/E4BP4 controls IgE class switching

The oncostatin M‐stromal cell axis in health and disease

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