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anti-Mouse (Murine) IL15 Antibodies:
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Human Monoclonal IL15 Primary Antibody for FACS - ABIN4897621
Anguille, Van Acker, Van den Bergh, Willemen, Goossens, Van Tendeloo, Smits, Berneman, Lion: Interleukin-15 Dendritic Cells Harness NK Cell Cytotoxic Effector Function in a Contact- and IL-15-Dependent Manner. in PLoS ONE 2015
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Human Monoclonal IL15 Primary Antibody for CyTOF, FACS - ABIN4900389
Marra, Mathew, Grigoriadis, Wu, Kyle-Cezar, Watkins, Rashid, De Rinaldis, Hessey, Gazinska, Hayday, Tutt: IL15RA drives antagonistic mechanisms of cancer development and immune control in lymphocyte-enriched triple-negative breast cancers. in Cancer research 2014
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Human Monoclonal IL15 Primary Antibody for FACS - ABIN4897620
Ferlazzo, Pack, Thomas, Paludan, Schmid, Strowig, Bougras, Muller, Moretta, Münz: Distinct roles of IL-12 and IL-15 in human natural killer cell activation by dendritic cells from secondary lymphoid organs. in Proceedings of the National Academy of Sciences of the United States of America 2004
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Human Polyclonal IL15 Primary Antibody for FACS, WB - ABIN4900388
Tejman-Yarden, Zlotnik, Lewis, Etzion, Chaimovitz, Douvdevani: Renal cells express a functional interleukin-15 receptor. in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2005
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Human Monoclonal IL15 Primary Antibody for - ABIN1383961
Bernard, Harb, Mortier, Quéméner, Meloen, Vermot-Desroches, Wijdeness, van Dijken, Grötzinger, Slootstra, Plet, Jacques: Identification of an interleukin-15alpha receptor-binding site on human interleukin-15. in The Journal of biological chemistry 2004
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Human Monoclonal IL15 Primary Antibody for FACS - ABIN4897618
Pangrazzi, Meryk, Naismith, Koziel, Lair, Krismer, Trieb, Grubeck-Loebenstein: "Inflamm-aging" influences immune cell survival factors in human bone marrow. in European journal of immunology 2017
Human Polyclonal IL15 Primary Antibody for Func, IHC (p) - ABIN2474939
Miller: T4 DNA polymerase (gene 43) is required in vivo for repair of gaps in recombinants. in Journal of virology 1975
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T cells in chimpanzees infected with human immunodeficiency virus express surface interleukin-15.
CD3(-) CD8(+) NK cells play a vital role in controlling HIV-1 infection by producing high levels of IFN-gamma, and that IL-15 elicits IFN-gamma production in this subpopulation of NK cells in HIV-1-infected chimpanzees. [Il-15, CD8 antigen, IFN-gamma]
these findings thus reveal a novel role for IL-15 in mediating gammadelta T cell localization within the intestinal mucosa and regulating gammadelta IEL motility and patrolling behavior as a critical component of host defense
the potential role of IL-15 as a modulator on fate of FAPs in injured muscle
these findings suggest that IL-15 reduces astrocyte loss and neuromyelitis optica pathology
IL-15 is a component of the inflammatory milieu in the tumor microenvironment promoting antitumor responses.
Here we focus on the cytokines implicated in thymic development of Treg(T lymphocytes (Treg) expressing the transcription factor Foxp3), with a particular emphasis on the roles of interleukin-2 and IL-15
intestinal IL-15 overexpression induces IL-18-dependent eosinophilia and immunoglobulins in the intestine that promotes food allergic responses.
SINTBAD regulates IL-15-induced autophagy and NKT cell survival.
this study shows that IL-15 supports the generation of protective lung-resident memory CD4 T cells
The small intestinal lamina propria innate lymphoid cells subset are not completely IL-7R dependent, but can persist partially through IL-15 signalling.
IL-15, mainly produced by non-hematopoietic cells in lung tissue and being trans-presented, promoted inflationary T cell survival by increasing expression of Bcl-2
This review provides significant characterization of specific systemic, cellular and molecular alterations caused by IL-15 superagonist treatment as compared to native IL-15 and compares their anti-tumor effectiveness in multiple preclinical studies [Review]
IL-15 trans-presentation by non-CD4 T cells is the primary mechanism via which IL-15 controls CD4 effector T cell differentiation.
the protective effect on metastasis was lost upon patrolling monocyte or NK cell depletion, IL15 neutralization, or IFNgamma ablation. The combined analysis of these approaches allowed us to establish a hierarchy in which patrolling monocytes, making IL15 in response to primary tumors, activate NK cells and IFNg production that then inhibit lung metastasis formation.
an IL-15 isoform lacking exon-6, IL-15DeltaE6, generated by alternative splicing events of activated immune cells, including macrophages and B cells, is reported.
IL-15, but not IL-15Ralpha, is required for the development of spontaneous and virus-induced Type 1 diabetes.
hetIL15 administration improves the outcome of Adoptive cell transfer in lymphoreplete hosts, a finding with significant implications for improving cell-based cancer immunotherapy strategies.
These data demonstrate that mice with an endogenous IL-15 deficiency are susceptible to the development of severe, enhanced Th2-mediated allergic airway disease, which can be regulated by CD8(+) T cells.
IL-15 induces the activation and survival of effector immune cells that are necessary for its antitumoral activity; but, long-term exposure to IL-15 is associated with the development of important side effects mainly mediated by IFN-gamma-producing T-cells
findings indicated that IL-15 plays an important role in preventing leukemia development.
NK cells activated by IL-4 in cooperation with IL-15 exhibit distinctive characteristics with enhanced immunologic cytotoxicity.
myotubes secrete IL-15 in response to TNFalpha stimulation supports the notion that IL-15 serves to mitigate inflammatory skeletal muscle loss.
this study shows that visceral adipose tissue produces IL-15 and may be a compensatory NK cell support mechanism in elderly human
The efficacy of future regimens may be improved by providing posttransfer support with IL2 or IL15.
IL-15 blood levels are higher in latent tuberculosis patients than in patients with active tuberculosis.
this study shows that the IL-15-AKT-XBP1s signaling pathway contributes to effector functions and survival in human NK cells
Our findings indicate that the synergism of T cells and sorafenib is mediated via reduced ATF4 expression, causing activation of the IRF7-IL-15 axis in leukemia cells and thereby leading to metabolic reprogramming of leukemia-reactive T cells in humans
More importantly, the recombinant fusion protein produced is fully active in stimulating T cell proliferation, when compared to the recombinant wild type IL15
IL-12 and IL-15 may be key for generating NK cells with a tissue-homing phenotype and strong Th1 cytokine profile in the blood, and links peripheral activation of NK cells with tissue-homing.
High IL15 expression is associated with follicles with immature oocytes.
IL-15 plays a pivotal role in creating a self-renewing, persistent HIV reservoir by facilitating infection of CD4(+) T cells with stem cell-like properties.
The genetic variations in IL15 affects the risk of developing of childhood acute lymphoblastic leukemia and are associated with hyperdiploidy in Latvian population.
circulating IL-15 and IL-15Ralpha concentrations are reduced in lean and obese physically active people
IL-15/IL-15Ralpha signaling pathway is activated in skeletal muscle in response to a session of resistance exercise.
Recipient IL-15 rs10519613 polymorphism was associated with hepatocellular carcinoma recurrence after liver transplantation.
iNKT cell development requires IL-15, and study found that sgammac interfered with IL-15 signaling to suppress iNKT cell generation in the thymus. Thus, sgammac represents a new mechanism to control cytokine availability during T cell development that constrains mature T cell production and specifically iNKT cell generation in the thymus.
The rs10833 polymorphism could be involved in regulating IL-15 production in subclinical atherosclerosis.
RFC, IL15 and VDR germline variants are associated with minimal residual disease in pediatric B-cell precursor ALL
IL-15 and IL-15Ralpha genes in samples from the Spanish Consortium for Genetics of Celiac Disease (CEGEC) collection, identifying two regulatory single-nucleotide polymorphisms (SNP) that might be associated with celiac disease
Study identified two completely linked SNPs in the porcine IL15 promoter region that could alter IL15 transcription activity. As interleukin-15 can inhibit porcine adipocyte differentiation, these promoter mutations could affect intramuscular fat deposition by producing differential levels of muscle-derived interleukin-15.
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 and NF-kappaB pathways
IFN-gamma 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 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.
IL 15 generates a dramatic expansion of short-lived memory CD8 T cells and natural killer in immunocompetent macaques and has long-term effects on the balance of CD4(+) and CD8(+) T cells.
These data suggest that therapeutic use of IL-15 in the setting of antiretroviral therapy might facilitate specific restoration of the CD4 + T cell compartment.
IL-15 secretion significantly correlates with the up-regulated expression of CD4 on memory CD4 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.