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Introduction

IL-38 is one of the members of the IL-1 family, which is the same as other IL-1 family members. It lacks signal peptide and caspase-1 cleavage site. IL-38 is widely expressed in immune tissues, such as spleen, thymus, tonsils, etc., and the expression is particularly obvious in skin and tonsil B cells. The expression level is low in the heart, placenta and other non-immune tissues. There is a certain connection between IL-38 and inflammation.

Mechanism and Function

The receptor of IL38 is IL-36R, and its binding ability is even stronger than IL-36Ra, so it plays a role in inflammation mainly through the IL-36Ra pathway. After the combination of Il-38 and IL-36R, it can inhibit the inflammatory pathway of NF-κB and mitogen-activated protein kinase(MAPKs). NF-κB has an effect on the activation of the mammalian target of rapamycin (mTOR), which leads to the influence on the phosphorylation of signal transducer and activator of transcription(STAT)3, which ultimately affects the differentiation of Th17.

In fact, IL-38 has many biological effects. For example, IL-38 has a biological basis as an IL-36R receptor antagonist, and its biological activity is similar to IL-36Ra. It can bind to IL-36R and induce its antagonism. IL-38 can inhibit the production of Th17-related cytokines IL-22 and IL-17 by blocking IL-1R and IL-36R signaling pathways, thereby playing an anti-inflammatory effect. Due to the "macrophage-apoptotic cell" interaction, IL-1 family proteins have the effect of regulating the production of macrophage cytokines. The binding of IL-1R6 and IL-1RAPL1 in the IL-1 receptor and IL-1 family is a necessary condition for the production of apoptosis-inducing cytokines in macrophages. It can reduce LPS, induce the production of IL-6 and IL-8, or inhibit the expression of IL-17 in THP-1 cells, so it plays a positive role in alleviating the inflammatory response under adjusted conditions. IL-38 can also cooperate with IL-36Ra to inhibit the production of IL-8 by peripheral blood mononuclear cells (PBMC) and increase the expression of IL-6.

IL-38 can participate in many diseases. For example, the abnormal expression of IL-38 is linked to the severity of autoimmune diseases. In Crohn, IL-38 expression increases in the synovium and colon of patients, inhibiting the binding of IL-36 and its receptor to protect the body. n K/BxN serum transfer-induced arthritis (STIA), overexpression of IL-38 can reduce collagen induced arthritis (CIA) and STIA's joint swelling and macrophage infiltration. IL-38 can also be seen in other inflammatory reactions. IL-38 is highly expressed in asthma, idiopathic pulmonary fibrosis and drug-induced pulmonary interstitial diseases. In addition, expression of IL-38 is quite high in atherosclerotic plaques. In addition to its effects on blood vessels, IL-38 can also inhibit endothelial cell proliferation and blood vessel formation stimulated by vascular endothelial growth factor (VEGF).

Mechanism of Signaling  Fig 1. Mechanism of Signaling

Creative Proteomics can provide cytokine detection platform for scientific research. According to different purposes, our dedicated analysts will customize exclusive solutions for you. We aim to provide customers with high-quality and convenient services to help you accelerate the progress of your project.

Our cytokine detection service includes but is not limited to:

Sample requirements

Our advantages:

Technology platform:

We mainly provide the Luminex cytokine detection platform. Luminex uses fluorescently encoded microspheres with specific antibodies to different target molecules. The different microspheres can be combined freely to a certain extent so that up to 100 analytes can be tested multiple times simultaneously in a single experiment.

The Luminex cytokine assay platform has the following advantages:

For your different needs, we can also provide the following detection methods:

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Mechanism of Signaling

For more information about the IL-38 detection service or need other detection requirements, please contact us.

References:

  1. Veerdonk F L V D, Stoeckman A K, Wu G, et al. IL-38 binds to the IL-36 receptor and has biological effects on immune cells similar to IL-36 receptor antagonist. Proceedings of the National Academy of Sciences of the United States of America, 2012, 109(8): p.3001-3005.
  2. Boutet M A, Najm, Aurélie, et al. IL-38 overexpression induces anti-inflammatory effects in mice arthritis models and in human macrophages in vitro. Annals of the Rheumatic Diseases, 2017:1304.
* For Research Use Only. Do Not use in diagnostic or therapeutic procedures.

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