Product nameFirePlex Human Inflammation - Immunoassay Panel
Sample typeCell culture supernatant, Saliva, Milk, Urine, Serum, Plasma, Other biological fluids, Heparin Plasma, EDTA Plasma, Citrate Plasma, Cerebral Spinal Fluid
Assay time3h 30m
Species reactivityReacts with: Human
Human Inflammation - Immunoassay Panel (ab229793) uses the FirePlex® particle technology to quantify up to 8 human proteins and peptides in the same well, from 12.5 µL sample input.
Assay run-time is 3.5 hours, followed by particle analysis using a validated flow cytometer model and data analysis using our integrated, free-of-charge FirePlex Analysis Workbench software.
Use of Inflammation - Multiplex Immunoassay Panel (ab229793) requires the purchase of
- A FirePlex Immunoassay Human Core Reagent Kit (ab208203)
- and FirePlex Immunoassay Protein Standard Mix A (ab227934)
FirePlex® is a registered trade mark in the United States and is registered as a European Union Trade Mark.
This panel was previously available under the product code ab213391, which is discontinued. We have redeveloped this panel using new, recombinant monoclonal antibodies that provide higher sensitivity and better reproducibility when quantifying the analytes with biofluid samples, improving consistency in kit performance.
The following information provides the sensitivity, range, CVs, required Protein Standard Mix and links to the individual target kit, where more information regarding recommeneded dilutions can be found.
Particle Code Protein
TNF alpha 5.36 4.57 - 10,000 1 Mix A IFN gamma 2.25 4.57 - 10,000 23 Mix A IL-1 beta 0.47 1.52 - 3,333 21 Mix A IL-6 0.15 0.51 - 1,111 9 Mix A IL-8 0.29 0.51 - 1,111 11 Mix A IL-10 1.12 4.57 - 10,000 13 Mix A IL-12p70 0.64 4.57 - 10,000 25 Mix A MCP1 0.28 1.52 - 3,333 31
Storage instructionsStore at -20°C. Please refer to protocols.
Components 1 x 96 tests 10X Human Inflammation Capture Particles (ab229793) 1 unit 15X Human Inflammation Biotin Detectors (ab229793) 1 unit
Cellular localizationIL12: Secreted. TNF alpha: Secreted and Cell membrane. IL8: Secreted. MCP1: Secreted. IL6: Secreted. IL10: Secreted. Interferon gamma: Secreted. IL1 beta: Cytoplasm, cytosol. Lysosome. Secreted, exosome. Cytoplasmic vesicle, autophagosome. Secreted. The precursor is cytosolic. In response to inflammasome-activating signals, such as ATP for NLRP3 inflammasome or bacterial flagellin for NLRC4 inflammasome, cleaved and secreted. IL1B lacks any known signal sequence and the pathway(s) of its secretion is(are) not yet fully understood (PubMed:24201029). On the basis of experimental results, several unconventional secretion mechanisms have been proposed. 1. Secretion via secretory lysosomes: a fraction of CASP1 and IL1B precursor may be incorporated, by a yet undefined mechanism, into secretory lysosomes that undergo Ca(2+)-dependent exocytosis with release of mature IL1B (PubMed:15192144). 2. Secretory autophagy: IL1B-containing autophagosomes may fuse with endosomes or multivesicular bodies (MVBs) and then merge with the plasma membrane releasing soluble IL1B or IL1B-containing exosomes (PubMed:24201029). However, autophagy impacts IL1B production at several levels and its role in secretion is still controversial. 3. Secretion via exosomes: ATP-activation of P2RX7 leads to the formation of MVBs containing exosomes with entrapped IL1B, CASP1 and other inflammasome components. These MVBs undergo exocytosis with the release of exosomes. The release of soluble IL1B occurs after the lysis of exosome membranes (By similarity). 4. Secretion by microvesicle shedding: activation of the ATP receptor P2RX7 may induce an immediate shedding of membrane-derived microvesicles containing IL1B and possibly inflammasome components. The cytokine is then released in the extracellular compartment after microvesicle lysis (PubMed:11728343). 5. Release by translocation through permeabilized plasma membrane. This may occur in cells undergoing pyroptosis due to sustained activation of the inflammasome (By similarity). These mechanisms may not be not mutually exclusive.
ab229793 has not yet been referenced specifically in any publications.