ARG82913

arigoPLEX^® Mouse M1/M2 Cytokines Multiplex ELISA Kit (IL4, IL6, IL10, TNF alpha)

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96 wells

699.00

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Overview

Product Description	ARG82913 arigoPLEX^® Mouse M1/M2 Cytokines Multiplex ELISA Kit (IL4, IL6, IL10, TNF alpha) is an Enzyme Immunoassay kit for the semi-quantification of IL4, IL6, IL10, TNF alpha in serum, plasma and cell culture supernatant. See all Multiplex ELISA kits
Tested Reactivity	Ms
Tested Application	ELISA
Target Name	Mouse M1/M2 Cytokines
Conjugation	HRP
Conjugation Note	Substrate: TMB and read at 450 nm
Sensitivity	IL4: 15.625 pg/ml IL6: 62.5 pg/ml IL10: 15.625 pg/ml TNF alpha: 31.25 pg/ml
Sample Type	Serum, plasma and cell culture supernatant.
Standard Range	IL4: 15.625 - 500 pg/ml IL6: 62.5 - 2000 pg/ml IL10: 15.625 - 500 pg/ml TNF alpha: 31.25 - 1000 pg/ml
Sample Volume	50 µl

Application Instructions

Assay Time	4 hour

Properties

Form	96 well
Storage Instruction	Store components at 4°C or -20°C. Keep microplate wells sealed in a dry bag with desiccants. Do not expose test reagents to heat, sun or strong light during storage and usage. Please refer to the product user manual for detail temperatures of the components.
Note	For laboratory research only, not for drug, diagnostic or other use.

Bioinformation

Database Links	GeneID: 21926 Mouse TNF Swiss-port # P06804 Mouse Tumor necrosis factor
Function	IL4: IL4 participates in at least several B-cell activation processes as well as of other cell types (PubMed:3016727). It is a costimulator of DNA-synthesis. It induces the expression of class II MHC molecules on resting B-cells. It enhances both secretion and cell surface expression of IgE and IgG1. It also regulates the expression of the low affinity Fc receptor for IgE (CD23) on both lymphocytes and monocytes. Positively regulates IL31RA expression in macrophages (By similarity). Stimulates autophagy in dendritic cells by interfering with mTORC1 signaling and through the induction of RUFY4 (By similarity). IL6: IL6 is a cytokine with a wide variety of biological functions in immunity, tissue regeneration, and metabolism. Binds to IL6R, then the complex associates to the signaling subunit IL6ST/gp130 to trigger the intracellular IL6-signaling pathway (Probable). The interaction with the membrane-bound IL6R and IL6ST stimulates 'classic signaling', whereas the binding of IL6 and soluble IL6R to IL6ST stimulates 'trans-signaling'. Alternatively, 'cluster signaling' occurs when membrane-bound IL6:IL6R complexes on transmitter cells activate IL6ST receptors on neighboring receiver cells (Probable). IL6 is a potent inducer of the acute phase response. Rapid production of IL6 contributes to host defense during infection and tissue injury, but excessive IL6 synthesis is involved in disease pathology. In the innate immune response, is synthesized by myeloid cells, such as macrophages and dendritic cells, upon recognition of pathogens through toll-like receptors (TLRs) at the site of infection or tissue injury (Probable). In the adaptive immune response, is required for the differentiation of B cells into immunoglobulin-secreting cells. Plays a major role in the differentiation of CD4+ T cell subsets. Essential factor for the development of T follicular helper (Tfh) cells that are required for the induction of germinal-center formation. Required to drive naive CD4+ T cells to the Th17 lineage. Also required for proliferation of myeloma cells and the survival of plasmablast cells. IL10: IL10 is a major immune regulatory cytokine that acts on many cells of the immune system where it has profound anti-inflammatory functions, limiting excessive tissue disruption caused by inflammation. Mechanistically, IL10 binds to its heterotetrameric receptor comprising IL10RA and IL10RB leading to JAK1 and STAT2-mediated phosphorylation of STAT3 (PubMed:16982608). In turn, STAT3 translocates to the nucleus where it drives expression of anti-inflammatory mediators (PubMed:18025162). Targets antigen-presenting cells (APCs) such as macrophages and monocytes and inhibits their release of pro-inflammatory cytokines including granulocyte-macrophage colony-stimulating factor /GM-CSF, granulocyte colony-stimulating factor/G-CSF, IL-1 alpha, IL-1 beta, IL-6, IL-8 and TNF-alpha (PubMed:1940799, PubMed:7512027, PubMed:11564774). Interferes also with antigen presentation by reducing the expression of MHC-class II and co-stimulatory molecules, thereby inhibiting their ability to induce T cell activation (PubMed:8144879). In addition, controls the inflammatory response of macrophages by reprogramming essential metabolic pathways including mTOR signaling (By similarity). TNF alpha: TNF alpha is a cytokine that binds to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, Under certain conditions it can stimulate cell proliferation and induce cell differentiation. Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Upregulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective (PubMed:23396208). Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line (PubMed:22517918, PubMed:16829952, PubMed:23396208). Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance (By similarity). Plays a role in angiogenesis by inducing VEGF production synergistically with IL1B and IL6 (PubMed:12794819). [provided by Uniprot]

Database Links

GeneID: 21926 Mouse TNF

Swiss-port # P06804 Mouse Tumor necrosis factor

Function

IL4: IL4 participates in at least several B-cell activation processes as well as of other cell types (PubMed:3016727).
It is a costimulator of DNA-synthesis. It induces the expression of class II MHC molecules on resting B-cells. It enhances both secretion and cell surface expression of IgE and IgG1. It also regulates the expression of the low affinity Fc receptor for IgE (CD23) on both lymphocytes and monocytes. Positively regulates IL31RA expression in macrophages (By similarity).
Stimulates autophagy in dendritic cells by interfering with mTORC1 signaling and through the induction of RUFY4 (By similarity).

IL6: IL6 is a cytokine with a wide variety of biological functions in immunity, tissue regeneration, and metabolism. Binds to IL6R, then the complex associates to the signaling subunit IL6ST/gp130 to trigger the intracellular IL6-signaling pathway (Probable). The interaction with the membrane-bound IL6R and IL6ST stimulates 'classic signaling', whereas the binding of IL6 and soluble IL6R to IL6ST stimulates 'trans-signaling'. Alternatively, 'cluster signaling' occurs when membrane-bound IL6:IL6R complexes on transmitter cells activate IL6ST receptors on neighboring receiver cells (Probable).
IL6 is a potent inducer of the acute phase response. Rapid production of IL6 contributes to host defense during infection and tissue injury, but excessive IL6 synthesis is involved in disease pathology. In the innate immune response, is synthesized by myeloid cells, such as macrophages and dendritic cells, upon recognition of pathogens through toll-like receptors (TLRs) at the site of infection or tissue injury (Probable). In the adaptive immune response, is required for the differentiation of B cells into immunoglobulin-secreting cells. Plays a major role in the differentiation of CD4+ T cell subsets. Essential factor for the development of T follicular helper (Tfh) cells that are required for the induction of germinal-center formation. Required to drive naive CD4+ T cells to the Th17 lineage. Also required for proliferation of myeloma cells and the survival of plasmablast cells.

IL10: IL10 is a major immune regulatory cytokine that acts on many cells of the immune system where it has profound anti-inflammatory functions, limiting excessive tissue disruption caused by inflammation. Mechanistically, IL10 binds to its heterotetrameric receptor comprising IL10RA and IL10RB leading to JAK1 and STAT2-mediated phosphorylation of STAT3 (PubMed:16982608).
In turn, STAT3 translocates to the nucleus where it drives expression of anti-inflammatory mediators (PubMed:18025162).
Targets antigen-presenting cells (APCs) such as macrophages and monocytes and inhibits their release of pro-inflammatory cytokines including granulocyte-macrophage colony-stimulating factor /GM-CSF, granulocyte colony-stimulating factor/G-CSF, IL-1 alpha, IL-1 beta, IL-6, IL-8 and TNF-alpha (PubMed:1940799, PubMed:7512027, PubMed:11564774).
Interferes also with antigen presentation by reducing the expression of MHC-class II and co-stimulatory molecules, thereby inhibiting their ability to induce T cell activation (PubMed:8144879).
In addition, controls the inflammatory response of macrophages by reprogramming essential metabolic pathways including mTOR signaling (By similarity).

TNF alpha: TNF alpha is a cytokine that binds to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, Under certain conditions it can stimulate cell proliferation and induce cell differentiation. Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Upregulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective (PubMed:23396208).
Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line (PubMed:22517918, PubMed:16829952, PubMed:23396208).
Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance (By similarity).
Plays a role in angiogenesis by inducing VEGF production synergistically with IL1B and IL6 (PubMed:12794819). [provided by Uniprot]

Specific References

Extracellular vesicle-guided in situ reprogramming of synovial macrophages for the treatment of rheumatoid arthritis

ELISA / Mouse/cell supernatants

Hyosuk Kim et al.
Biomaterials, (2022)

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ARG82913 arigoPLEX^® Mouse M1/M2 Cytokines multiplex ELISA Kit (IL4, IL6, IL10, TNF alpha) User manual	Download

Inflammation

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Inflammasome & Pyroptosis

ARG82913

arigoPLEX® Mouse M1/M2 Cytokines Multiplex ELISA Kit (IL4, IL6, IL10, TNF alpha)

arigoPLEX® Mouse M1/M2 Cytokines Multiplex ELISA Kit (IL4, IL6, IL10, TNF alpha) for ELISA and Mouse

arigoPLEX^® Mouse M1/M2 Cytokines Multiplex ELISA Kit (IL4, IL6, IL10, TNF alpha)

arigoPLEX^® Mouse M1/M2 Cytokines Multiplex ELISA Kit (IL4, IL6, IL10, TNF alpha) for ELISA and Mouse