- Catalogue N°
- 874.082.001 - 1 x 96 Discovery (plate not included)
874.082.001P - 1 x 96 Discovery (non-sterile plate)
874.082.001S - 1 x 96 Discovery (sterile plate)
874.082.005 - 5 x 96 (plates not included)
874.082.005P - 5 x 96 (non-sterile plates)
874.082.005S - 5 x 96 (sterile plates)
874.082.010 - 10 x 96 (plates not included)
874.082.010P - 10 x 96 (non-sterile plates)
874.082.010S - 10 x 96 (sterile plates)
874.082.015 - 15 x 96 (plates not included)
874.082.015P - 15 x 96 (non-sterile plates)
874.082.015S - 15 x 96 (sterile plates)
874.082.020 - 20 x 96 (plates not included)
874.082.020P - 20 x 96 (non-sterile plates)
874.082.020S - 20 x 96 (sterile plates)
- Target species
- Recognizes natural human IFN-g and IL-17A
- 3h30 after cell stimulation
- Cross Reaction
- No cross reactivity with other human cytokines
- Kit Content
- Diaclone Dual Fluorospot Sets include Capture antibody for cytokine 1, FITC-conjugated detection antibody for cytokine 1, anti-FITC antibody green fluorescence conjugate, capture antibody for cytokine 2, biotinylated detection antibody for cytokine 2, streptavidin-phycoerythrin conjugate, BSA.
IFNg, also called Type II interferon, is a homodimeric glycoprotein containing approximately 21 to 24 kD subunits. The human IFNg gene, situated on chromosome 12, contains three introns; the four exons code for a polypeptide of 166 amino acids, 20 of which constitute the signal peptide. In contrast to IFNa and IFNb synthesis, which can occur in any cell, production of IFNg is a function of T cells and NK cells. All IFNg inducers activate T cells either in a polyclonal (mitogens or antibodies) or in a clonally restricted, antigen-specific, manner. IFNg is produced during infection by T cells of the cytotoxic/suppressor phenotype (CD8) and by a subtype of helper T cells, the Th1 cells. Th1 cells secrete IL-2, IL-3, TNFa and IFNg, whereas Th2 cells main produce IL-3, IL-4, IL-5, and IL-10, but little or no IFNg. IFNg preferentially inhibits the proliferation of Th2 but not Th1 cells, indicating that the presence of IFNg during an immune response will result in the preferential proliferation of Th1 cells .
Type II IFN or IFNg is a lymphokine that displays no molecular homology with type I IFN, but shares some important biologic activities. Specifically, IFNg induces an anti-viral state and is anti-proliferative. In addition, IFNg has several properties related to immunoregulation.
1) IFNg is a potent activator of mononuclear phagocytes, e.g. IFNg stimulates the expression of Mac-1, augments endocytosis and phagocytosis by monocytes, and activates macrophages to kill tumor cells by releasing reactive oxygen intermediates and TNFa.
2) IFNg induces or augments the expression of MHC antigens on macrophages, T and B cells and some tumor cell lines.
3) On T and B cells IFNg promotes differentiation. It enhances proliferation of activated B cells and can act synergistically with IL-2 to increase immunoglobulin light-chain synthesis . IFNg is one of the natural B-cell differentiation factors.
4) Finally, IFNg activates neutrophils, NK cells and vascular endothelial cells.
The role of IFNg as a disease marker has been demonstrated for a number of different pathological situations:
- IFNg is produced during viral infections. IFNg is a diagnostic tool for distinguishing tuberculous from other non-tuberculous ascites . IFNg values in pleural fluid are significantly higher in tuberculous pleuritis patients than those in non-tuberculous pleuritis patients, with a sensitivity and a specificity of 100%. Therapy-induced (treatment with thalidomide) alleviation of clinical symptoms of erythema nodosum leprosum correlates with IFNg and TNFa levels. Tuberculoid leprosy patients show increased lymphocyte proliferation and IFNg production in response to stimulation with Mycobacterium leprae as compared to lepromatous leprosy patients and healthy individuals.
- Autoimmune diseases: Accurate measurements of cellular production of cytokines, e.g. IFNg is important in the design and monitoring of immunotherapy of multiple sclerosis.
- Transplant rejection: Intragraft IFNg mRNA expression occurs in active acute transplant rejection preceding clinical transplant rejection, thus offering an early diagnostic tool for detection of transplant rejection.
- IFNg production by isolated lymphocytes is not detectable in patients with cow's milk allergy as compared to control individuals. Infants who develop atopy produce significantly less IFNg at birth compared to infants who do not develop atopy.
- Peripheral blood lymphomononuclear cells from newly diagnosed type I diabetes produce significantly less IFNg in comparison to controls and long standing diabetes.
Classically following antigenic stimulation and regulation by specific co-stimulatory molecules Naïve CD4+ T-cells where known to differentiate into Th1 and Th2 cells. However in recent years the identification of IL-17 and IL-23 has led to the classification of a third subset of the Th cell family, Th17 cells. These cells are classified on their ability to secrete IL-17A but not IFNg and IL-4 the main effector cytokines of Th1 and Th2 cells.
IL-17A was originally identified as a transcript from a rodent T-cell hybridoma by Rouvier et al. in 1993 and also called CTLA-8. IL-17A is a homodimeric glycoprotein consisting of 155 amino acids and has a molecular weight of 35kDa.
IL-17A links innate and adaptive immunity and has both beneficial and pathological effects on the immune system. IL-17A is involved in inducing and mediating proinflammatory responses, commonly associated with allergic responses and induces the production of many other cytokines (such as IL-6, G-CSF, GM-CSF, IL-1β, TGFβ, TNFα), chemokines (including IL-8, GRO-α and MCP-1) and prostaglandins (e.g. PGE2) from many cell types (fibroblasts, endothelial cells, epithelial cells, keratinocytes and macrophages). In-vivo studies have now indicated that IL-17A is an especially potent activator of neutrophils. IL-17A has been shown to play an important role in the host immune response to various infection and disease states, including bacterial, fungal and viral infections, autoimmune disease including psoriasis, rheumatoid arthritis (increased levels in the synovial fluid) and multiple sclerosis as well as inflammatory conditions such as Crohn’s disease.
Version 4 - 07.19
For research use only
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