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CartSwine IFN gamma Do-It-Yourself ELISA, ≤10 Plates
Swine IFN-γ ELISA Data
Swine IFN-γ ELISA Kit Components
| Component | Usage | Quantity | Catalog # |
| Anti-Swine IFNγ Polyclonal Antibody | Capture Antibody | 100 µg | PB0157S-100 |
| Biotinylated Anti-Swine IFNγ Polyclonal Antibody | Detection Antibody | 50 µg | PBB0269S-050 |
| Swine IFNγ Recombinant Protein | Standard | 5 µg | RP0126S-005 |
Swine IFN-γ ELISA Specifications
The Swine IFNγ Do-It-Yourself ELISA contains capture antibody, standard, and detection antibody for development of a Swine IFNγ ELISA. The antibodies have been determined to function in an ELISA with the standard provided. Optimal buffers, concentrations, incubation times, incubation temperatures, and methods for the ELISA have not been determined. A working knowledge of ELISA is strongly recommended. The quantities of components provided are not matched. Components may also be purchased separately.
For additional tips and techniques to ensure a successful ELISA, check out our ELISA Technical Guide.
IFN-γ Background
Interferon-gamma (IFN-γ) is a dimerized soluble cytokine that is the only member of the type II class of interferons. This interferon was originally called macrophage-activating factor, a term now used to describe a larger family of proteins to which IFN-γ belongs. IFN-γ, or type II interferon, is a cytokine that is critical for innate and adaptive immunity against viral and intracellular bacterial infections and for tumor control. Aberrant IFN-γ expression is associated with a number of autoinflammatory and autoimmune diseases. The importance of IFN-γ in the immune system stems in part from its ability to inhibit viral replication directly, but, most important, derives from its immunostimulatory and immunomodulatory effects. IFN-γ is produced predominantly by natural killer (NK) and natural killer T (NKT) cells as part of the innate immune response, and by CD4 and CD8 cytotoxic T lymphocyte (CTL) effector T cells once antigen-specific immunity develops.
Alternate Names - IFNG, IFG, IFI, interferon, gamma, interferon gamma
Changes in Glomerular Filtration Rate After Renal Revascularization Correlate With Microvascular Hemodynamics and Inflammation in Swine Renal Artery Stenosis.
Eirin A, Ebrahimi B, Zhang X, Zhu XY, Tang H, Crane JA, Lerman A, Textor SC, Lerman LO.
Circ Cardiovasc Interv. 2012 Oct 9.
Applications: Measurement of Swine MCP-1 (CCL2), IFN gamma, and IL-17A in plasma by ELISA.
BACKGROUND:
The selection of patients with renal artery stenosis (RAS) likely to improve glomerular filtration rate (GFR) after percutaneous transluminal renal angioplasty is difficult. We examined basal hemodynamic and inflammatory factors linked to improved stenotic kidney (STK) function after percutaneous transluminal renal angioplasty in swine RAS.
METHODS AND RESULTS:
Fifteen pigs after 6 weeks of hemodynamically significant RAS were studied before and 4 weeks after technically successful percutaneous transluminal renal angioplasty+stenting. STK and contralateral kidney hemodynamics and function were evaluated by multidetector computed-tomography before and after acetylcholine challenge. Single-kidney deoxyhemoglobin (R2*, reciprocal to blood relaxation) and energy-dependent tubular function were assessed using blood-oxygen-level-dependent magnetic resonance imaging before and after furosemide. Baseline renal vein and inferior vena cava levels of inflammatory markers were measured and their gradient and net release calculated. Baseline parameters were compared with normal (n=7) and sham-RAS (n=7) pigs and correlated with the change in STK-GFR after revascularization (ΔGFR). Four weeks after percutaneous transluminal, renal angioplasty blood pressure was normalized in all animals, but STK-GFR improved in 10 of 15 (ΔGFR =+22.0±8.5 mL/min). ΔGFR correlated inversely with basal STK-GFR, renal release of inflammatory markers, and medullary R2* response to furosemide, but directly with GFR response to acetylcholine. Basal contralateral kidney GFR correlated directly with ΔGFR.
CONCLUSIONS:
Low basal STK-GFR with preserved response to acetylcholine may predict benefit from revascularization in RAS, whereas renal inflammation and robust STK-R2* responses to furosemide (possibly reflecting avid tubular oxygen consumption) are associated with less favorable outcomes. These tools may be useful for identification of patients likely to improve renal function after revascularization.
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