- Catalogue N°
- 867.011.001 - 1 x 96 Discovery (plate not included)
867.011.001P - 1 x 96 Discovery (non-sterile plate)
867.011.001S - 1 x 96 Discovery (sterile plate)
867.011.005 - 5 x 96 (plates not included)
867.011.005P - 5 x 96 (non-sterile plates)
867.011.005S - 5 x 96 (sterile plates)
867.011.010 - 10 x 96 (plates not included)
867.011.010P - 10 x 96 (non-sterile plates)
867.011.010S - 10 x 96 (sterile plates)
867.011.015 - 15 x 96 (plates not included)
867.011.015P - 15 x 96 (non-sterile plates)
867.011.015S - 15 x 96 (sterile plates)
867.011.020 - 20 x 96 (plates not included)
867.011.020P - 20 x 96 (non-sterile plates)
867.011.020S - 20 x 96 (sterile plates)
- Target species
- Recognizes natural rat IFN-g
- 3h after cell stimulation
- Cross Reaction
- No cross reactivity with other rat cytokines
- Kit Content
- Diaclone ELISpot Sets include capture and detection antibodies, Streptavidin - Alkaline Phosphatase conjugated, BSA, BCIP/NTB and blocking reagent.
- Additional Information
- Spots read visually or with reader
Different populations of T-cells secrete differing patterns of cytokines that ultimately lead to different immune responses. IFNg production is a key function of Th1, CD8+ CTLs and also NK cells. IFN-g is a cytokine critical for cell mediated immunity against viral and intracellular bacterial infections and is involved in the inflammatory response following secretion via macrophage activation and stimulation of antibody secretion. IFNg is the hallmark effector cytokine of Th1 and therefore is an excellent marker for identifying a host response to intracellular pathogens.
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 mainly produce IL-3, IL-4, IL-5 and IL-10, but little or no IFNg (1). 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 (2).
In addition, IFNg has several properties related to immunoregulation. IFNg is a potent activator of mononuclear phagocytes (3), and activates macrophages to kill tumor cells by releasing reactive oxygen intermediates and TNFa (4). IFNg induces or augments the expression of MHC antigens on macrophages, T and B cells and some tumor cell lines (5). 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 (6, 7).
The role of IFNg as a disease marker has been demonstrated for a number of different pathological situations including, viral infection (8), Autoimmune disease (9), transplant rejection (10), Diabetes (5) and allergy (11).
Version 7 - 02.18
For research use only
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