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IL-32 Detection (CAT#: STEM-MB-0298-WXH)

Introduction

Interleukin 32, also known as natural killer factor 4, is a class of cytokines containing multiple splice variants, which is closely related to many inflammatory and autoimmune diseases. IL-32 is mainly produced by natural killer cells, T cells, epithelial cells, and monocytes in the surrounding blood. Interferon (IFN) -γ can strongly induce the production of IL-32 in epithelial cells and monocytes. There are many splicing variants of IL-32. Its main biological characteristics include the induction of inflammatory cytokines, the promotion of inflammatory mediator release, and the regulation of the normal function of natural killer cells. Studies have shown that IL-32 exhibits the characteristics of pro-inflammatory factors, can promote the secretion of multiple inflammatory factors such as IL-6, IL-1β, TNF-α, and has a cascade amplification effect. In addition, IL-32 is closely related to inflammatory diseases such as rheumatoid arthritis (RA), Crohn disease, tuberculosis, acquired immune deficiency syndrome, and the expression of IL-32 is also related to the rate of red blood cell sedimentation.




Principle

IL-32 binding enzyme 3 (PR3) has high affinity and cannot be inhibited by enzymes, and is one of the receptors of IL-32. PR3 is a neutrophil serine protease and exists in a soluble or thin film form. PR3 is a specific IL-32α binding protein and does not depend on enzyme activity. Increasing the activity of cytokines by PR3 can limit the division of IL-32α. Therefore, treatment of IL-32 by specific inhibition of PR3 activity or neutralization of IL-32 by inactive PR3 can reduce the consequences of the effects of IL-32 in immunomodulatory diseases. It may be a good strategy to combat PR3 enzyme activity and select PR3 through enzyme inactivation to block IL-32 in the diseases in which IL-32 is involved.

Applications

IL-32 can exert antitumor effects.
IL-32 can induce T cell apoptosis, damage the immune monitoring function of NK cells, and induce monocytes to differentiate into macrophage-like cells.
IL-32 can affect the expression of anti-apoptotic proteins BcI-2, BcI-xL and McI-1.

Procedure

1. Process samples.
2. IL-32 detection (qPCR, Enzyme-linked immunosorbent assay (ELISA), Flow cytometry).
3. Analysis results.

Notes

Sample Types-Blood, serum, plasma, cerebrospinal fluid, cell culture supernatant, tissue homogenate, cell culture medium, urine, tumor, etc.

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