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Rat (Rattus) IL15 ELISA Kit for Sandwich ELISA - ABIN365261
Zanchi, Lira, de Siqueira Filho, Rosa, de Oliveira Carvalho, Seelaender, Santos, Lancha: Chronic low frequency/low volume resistance training reduces pro-inflammatory cytokine protein levels and TLR4 mRNA in rat skeletal muscle. in European journal of applied physiology 2010
Show all 2 references for ABIN365261
Human IL15 ELISA Kit for Sandwich ELISA - ABIN414877
Shi, Liu, Zhang, Guo, Song, Song, Liu: miR-15b is Downregulated in Myasthenia Gravis Patients and Directly Regulates the Expression of Interleukin-15 (IL-15) in Experimental Myasthenia Gravis Mice. in Medical science monitor : international medical journal of experimental and clinical research 2015
Mouse (Murine) IL15 ELISA Kit for Sandwich ELISA - ABIN365238
Yin, Xu, Sun, Wei, Tian: Interleukin-15 suppresses hepatitis B virus replication via IFN-? production in a C57BL/6 mouse model. in Liver international : official journal of the International Association for the Study of the Liver 2012
T cells in chimpanzees infected with human immunodeficiency virus express surface interleukin-15.
CD3 (show CD3 ELISA Kits)(-) CD8 (show CD8A ELISA Kits)(+) NK cells play a vital role in controlling HIV-1 infection by producing high levels of IFN-gamma (show IFNG ELISA Kits), and that IL-15 elicits IFN-gamma (show IFNG ELISA Kits) production in this subpopulation of NK cells in HIV-1-infected chimpanzees. [Il-15, CD8 (show CD8A ELISA Kits) antigen, IFN-gamma (show IFNG ELISA Kits)]
this study shows that synergistic enhancement of adaptive immunity by the combination of epigallo catechin gallate and vitamin A or E is dependent on both IL-15 and its receptor
Under steady-state conditions, KLF2 (show KLF2 ELISA Kits)-deficient NK cells alter their expression of homeostatic homing receptors and subsequently undergo apoptosis due to IL-15 starvation.
The induction of IgM (show CD40LG ELISA Kits) and IgA, which can play pivotal roles in mucosal immunity, was promoted in the presence of IL-15. Collectively, the data implicate IL-15 as the master cytokine that induces B-1a cells to mount a mucosal immune response.
The novel mechanism of IL-15 transfer to the surface of antigen-processing DCs may explain the enhanced potency of IL-15:IL-15Ralpha-coated nanoparticles for antigen delivery.
Muscle FNDC5 (show FNDC5 ELISA Kits) mRNA expression and irisin (show FNDC5 ELISA Kits) release are not IL-15-dependent in mice.
Virtual memory T cells develop and mediate bystander protective immunity in an IL-15-dependent manner.
Impaired delivery of IL-15 to CD4 (show CD4 ELISA Kits)+ T cells in the colon downmodulates Foxp3 (show FOXP3 ELISA Kits) expression and enhances RORgammat expression. CD4 (show CD4 ELISA Kits)+ T cells deprived of IL-15 trigger IBD characterized by production of pro-inflammatory cytokines and accumulation of Th1 (show HAND1 ELISA Kits)/Th17 cells.
Most (86%) IL15 in serum resides in the free state, with a minor proportion (14%) residing in complex with IL15Ralpha. Results suggest that IL15 is released as a free molecule by an unknown mechanism rather than via cleavage of membrane-bound IL15/IL15Ralpha.
IL-15 may influence mononuclear phagocytes subsets in the gut (show GUSB ELISA Kits) in a novel way that alters the frequency of lamina propria Th17 cells.
Downregulation of STAT3 (show STAT3 ELISA Kits) phosphorylation enhances tumoricidal effect of IL-15-activated dendritic cell against doxorubicin-resistant lymphoma and leukemia via TNF-alpha (show TNF ELISA Kits).
Cutaneous T-cell lymphoma (CTCL (show TSPYL2 ELISA Kits)) pathogenesis remains unknown, and there are no curative therapies. Our findings not only demonstrate a critical role for IL15-mediated inflammation in cutaneous T-cell lymphomagenesis, but also uncover a new oncogenic regulatory loop in CTCL (show TSPYL2 ELISA Kits) involving IL15, HDAC1 (show HDAC1 ELISA Kits), HDAC6 (show HDAC6 ELISA Kits), and miR (show MLXIP ELISA Kits)-21 that shows differential sensitivity to isotype-specific HDAC (show HDAC3 ELISA Kits) inhibitors
we provide the first direct evidence that IL-15 is expressed both at the mRNA and protein level in human salivary gland epithelial cells and it is clear that salivary glands from primary Sjogren's syndrome patients showed an intensified epithelial expression of IL-15
Data show a greater expression of interleukin 15 (IL-15) mRNA in healing wounds compared with non-healing wounds.
Our study indicates that the IL15 +96522A/C polymorphism correlates with the severity of Hashimoto's disease (HD), most likely by increasing Th17 cells.
this study shows that IL-15 induces cytokine-induced killer cells with a potent cytotoxic activity mostly against tumor cells from epithelial solid malignancies via NKG2D (show KLRK1 ELISA Kits)-mediated mechanism.
IL-15 is able to significantly regulate the inflammatory infiltration of macrophages in polymyositis patients through affecting the NF-kB pathway and MMP-9 (show MMP9 ELISA Kits) expression levels.
IL-15 mRNA expression was significantly higher in patients with moderately severe viral bronchiolitis compared to controls and patients with severe disease. Serum IL15 correlated with disease severity.
These data underline the potential of "free" IL15 in the absence of Ralpha-complex as a powerful and specific immuno-modulator, which may be beneficial where selective immune-activation is desired.
Data indicate that high interleukin-16 (show IL16 ELISA Kits) (IL-6 (show IL6 ELISA Kits)), interferon-gamma (IFN-gamma (show IFNG ELISA Kits)) and low interleukin-15 (IL-15) levels suggest active tuberculosis.
Culturing NK cells under hypoxia compared with ambient air (normoxia) and IL-15 priming synergistically augmented glycolytic gene expression without major changes in glycolytic flux and glucose consumption.
Myokine IL-15 regulates the crosstalk of co-cultured porcine skeletal muscle satellite cells and preadipocytes.
results demonstrate that porcine reproductive and respiratory syndrome virus (PRRSV)infection could induce IL-15 production in macrophages/dendritic cells; data further show that upregulation of IL-15 by PRRSV requires PKC (show FYN ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits) pathways
IFN-gamma (show IFNG ELISA Kits) targets the adipocyte to induce IL-15 expression, thus indicating a possible role for the adipocyte in the regulation of T-cell function and muscle metabolism during the innate immune response
When induced by IFN-gamma (show IFNG ELISA Kits) or other inflammatory mediators, IL-15 may be a significant homeorhetic factor that mobilizes and directs energy away from the adipocyte to other cells during the acute phase of the inflammatory response.
Increased function and survival of IL-15-transduced dendritic cells are mediated by up-regulation of IL-15Ralpha and Bcl-2 (show BCL2 ELISA Kits).
IL 15 generates a dramatic expansion of short-lived memory CD8 (show CD8A ELISA Kits) T cells and natural killer in immunocompetent macaques and has long-term effects on the balance of CD4 (show CD4 ELISA Kits)(+) and CD8 (show CD8A ELISA Kits)(+) T cells.
These data suggest that therapeutic use of IL-15 in the setting of antiretroviral therapy might facilitate specific restoration of the CD4 (show CD4 ELISA Kits) + T cell compartment.
IL-15 secretion significantly correlates with the up-regulated expression of CD4 (show CD4 ELISA Kits) on memory CD4 (show CD4 ELISA Kits) T cells that is associated with increased permissiveness to simian immunodeficiency virus infection.
The protein encoded by this gene is a cytokine that regulates T and natural killer cell activation and proliferation. This cytokine and interleukine 2 share many biological activities. They are found to bind common hematopoietin receptor subunits, and may compete for the same receptor, and thus negatively regulate each other's activity. The number of CD8+ memory cells is shown to be controlled by a balance between this cytokine and IL2. This cytokine induces the activation of JAK kinases, as well as the phosphorylation and activation of transcription activators STAT3, STAT5, and STAT6. Studies of the mouse counterpart suggested that this cytokine may increase the expression of apoptosis inhibitor BCL2L1/BCL-x(L), possibly through the transcription activation activity of STAT6, and thus prevent apoptosis. Alternatively spliced transcript variants of this gene have been reported.