arigoPLEX® Mouse Th1/Th2/Th17/Treg Cytokines Multiplex ELISA Kit (IFN gamma, IL4, IL17, IL10)

arigoPLEX® Mouse Th1/Th2/Th17/Treg Cytokines Multiplex ELISA Kit (IFN gamma, IL4, IL17, IL10) is an Enzyme Immunoassay kit for the semi-quantification of IFN gamma, IL4, IL17, IL10 in serum, plasma and cell culture supernatant.

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Background

Th1 helper cells lead to an increased cell-mediated response (primarily by macrophages and cytotoxic T cells), typically against intracellular bacteria and protozoa. They are triggered by the polarising cytokine IL-12 and their effector cytokines are IFN-gamma and IL-2. Th2 helper cells lead to a humoral immune response, typically against extracellular parasites such as helminths. They are triggered by the polarising cytokines IL-4 and IL-2, and their effector cytokines are IL-4, IL-5, IL-9, IL-10, IL-13 and IL-25. Th17 helper cells are a subset of T helper cells developmentally distinct from Th1 and Th2 lineages producing interleukin 17 (IL-17). The cells produce IL-17 which is a pro-inflammatory substance. This means it is especially good at fighting extracellular pathogens and fungi. [Provided by Wikipedia: T helper cell]

IFN gamma: Type II interferon produced by immune cells such as T-cells and NK cells that plays crucial roles in antimicrobial, antiviral, and antitumor responses by activating effector immune cells and enhancing antigen presentation.
Primarily signals through the JAK-STAT pathway after interaction with its receptor IFNGR1 to affect gene regulation.
Upon IFN gamma binding, IFNGR1 intracellular domain opens out to allow association of downstream signaling components JAK2, JAK1 and STAT1, leading to STAT1 activation, nuclear translocation and transcription of IFNG-regulated genes. Many of the induced genes are transcription factors such as IRF1 that are able to further drive regulation of a next wave of transcription.
IFN gamma plays a role in class I antigen presentation pathway by inducing a replacement of catalytic proteasome subunits with immunoproteasome subunits.

IL4: IL4 participates in at least several B-cell activation processes as well as of other cell types.
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.
Stimulates autophagy in dendritic cells by interfering with mTORC1 signaling and through the induction of RUFY4.

IL17A: IL17A is an effector cytokine of innate and adaptive immune system involved in antimicrobial host defense and maintenance of tissue integrity.
Signals via IL17RA-IL17RC heterodimeric receptor complex, triggering homotypic interaction of IL17RA and IL17RC chains with TRAF3IP2 adapter. This leads to downstream TRAF6-mediated activation of NF-kappa-B and MAPkinase pathways ultimately resulting in transcriptional activation of cytokines, chemokines, antimicrobial peptides and matrix metalloproteinases, with potential strong immune inflammation.
Plays an important role in connecting T cell-mediated adaptive immunity and acute inflammatory response to destroy extracellular bacteria and fungi. As a signature effector cytokine of T-helper 17 cells (Th17), primarily induces neutrophil activation and recruitment at infection and inflammatory sites.

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.
In turn, STAT3 translocates to the nucleus where it drives expression of anti-inflammatory mediators.
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.
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. [Provided by Uniprot]

Target Information