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anti-Mouse (Murine) IL15 Anticorps:
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Human Monoclonal IL15 Primary Antibody pour 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. dans PLoS ONE 2015
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Human Monoclonal IL15 Primary Antibody pour 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. dans Cancer research 2014
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Human Monoclonal IL15 Primary Antibody pour - 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. dans The Journal of biological chemistry 2004
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Human Monoclonal IL15 Primary Antibody pour 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. dans Proceedings of the National Academy of Sciences of the United States of America 2004
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Human Polyclonal IL15 Primary Antibody pour FACS, WB - ABIN4900388
Tejman-Yarden, Zlotnik, Lewis, Etzion, Chaimovitz, Douvdevani: Renal cells express a functional interleukin-15 receptor. dans Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2005
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Human Polyclonal IL15 Primary Antibody pour Func, IHC (p) - ABIN2474939
Miller: T4 DNA polymerase (gene 43) is required in vivo for repair of gaps in recombinants. dans Journal of virology 1975
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Human Monoclonal IL15 Primary Antibody pour FACS - ABIN4897618
Pangrazzi, Meryk, Naismith, Koziel, Lair, Krismer, Trieb, Grubeck-Loebenstein: "Inflamm-aging" influences immune cell survival factors in human bone marrow. dans European journal of immunology 2017
T cells in chimpanzees infected with human immunodeficiency virus express surface interleukin-15.
CD3 (Montrer CD3 Anticorps)(-) CD8 (Montrer CD8A Anticorps)(+) NK cells play a vital role in controlling HIV-1 infection by producing high levels of IFN-gamma (Montrer IFNG Anticorps), and that IL-15 elicits IFN-gamma (Montrer IFNG Anticorps) production in this subpopulation of NK cells in HIV-1-infected chimpanzees. [Il-15, CD8 (Montrer CD8A Anticorps) antigen, IFN-gamma (Montrer IFNG Anticorps)]
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 (Montrer BCL2 Anticorps)
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 (Montrer CD4 Anticorps) T cells is the primary mechanism via which IL-15 controls CD4 (Montrer CD4 Anticorps) 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 (Montrer IFNG Anticorps) 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.
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 (Montrer CD8A Anticorps)(+) 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 (Montrer IFNG Anticorps)-producing T-cells
findings indicated that IL-15 plays an important role in preventing leukemia development.
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 (Montrer CD4 Anticorps)(+) 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
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 (Montrer FYN Anticorps) and NF-kappaB (Montrer NFKB1 Anticorps) pathways
IFN-gamma (Montrer IFNG Anticorps) 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 (Montrer IFNG Anticorps) 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 (Montrer BCL2 Anticorps).
IL 15 generates a dramatic expansion of short-lived memory CD8 (Montrer CD8A Anticorps) T cells and natural killer in immunocompetent macaques and has long-term effects on the balance of CD4 (Montrer CD4 Anticorps)(+) and CD8 (Montrer CD8A Anticorps)(+) T cells.
These data suggest that therapeutic use of IL-15 in the setting of antiretroviral therapy might facilitate specific restoration of the CD4 (Montrer CD4 Anticorps) + T cell compartment.
IL-15 secretion significantly correlates with the up-regulated expression of CD4 (Montrer CD4 Anticorps) on memory CD4 (Montrer CD4 Anticorps) 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.