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Human Anti-IFN-alpha ELISA

  • Regulatory status:RUO
  • Type:Sandwich ELISA, HRP-labelled antibody
  • Other names:Anti-alpha interferon, IFN leukocytic, LeIF D
  • Species:Human
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Cat. No. Size Price


RAF003R 96 wells (1 kit)
PubMed Product Details
Technical Data

Type

Sandwich ELISA, HRP-labelled antibody

Description

The human anti-IFN-alpha ELISA is an enzyme-linked immunosorbent assay for the quantitative detection of human anti-IFN-alpha. The human anti-IFN-alpha ELISA is for research use only.

Applications

Serum, Urine, Plasma, Cell culture supernatant

Sample Requirements

20 µl/well

Shipping

On blue ice packs. Upon receipt, store the product at the temperature recommended below.

Storage/Expiration

Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Curve

Calibration Range

3.1 –200 ng/ml

Limit of Detection

1.4 ng/ml

Intra-assay (Within-Run)

CV = 3.3%

Inter-assay (Run-to-Run)

CV = 4.1%

Spiking Recovery

92,00%

Dilution Linearity

104,00%

Summary

Features

  • RUO
  • sensitivity 1.4 ng/ml
  • intraassay CV = 3.3%
  • interassay CV = 4.1%
  • standard curve: 3.1 - 200 ng/ml

Research topic

Autoimmunity, Cytokines and chemokines and related molecules, Immune Response, Infection and Inflammation

Summary

Studies on antigenicity led to the concept that molecules like the interferons were not immunogenic in homologous systems because antibodies are not normally produced against "self" antigens. However, naturally occuring or therapeutically induced antibodies to cytokines such as interferons, tumor necrosis factors (TNF), interleukins (IL) and various growth factors were found, which are generally thought to inhibit cytokine functions, and the appearance of such antibodies should therefore result in various degrees of cytokine deficiency. It is a common concept that the development of antibodies against any auto-antigen or drug is always undesirable. Such antibodies are crucial for the pathology of autoimmune diseases and inhibit the pharmacological effects of drugs including exogenously administered cytokines.

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