ArticleMethods in molecular biology (Clifton, N.J.)2023
Dissecting Interleukin-6 Classic and Trans-signaling in Inflammation and Cancer.
Article in Methods in molecular biology (Clifton, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- The Bidirectional Regulatory Role of Neuroimmune Interaction in Neurodevelopment and Neurodegenerative Diseases.The Yale journal of biology and medicine · 2026Review
- Insights into IL-6/JAK/STAT3 signaling in the tumor microenvironment: Implications for cancer therapy.Cytokine & growth factor reviews · 2025Review
- Exploring the mechanisms of Chaige Kangyi Recipe in treating recurrent pregnancy loss with insulin resistance.Scientific reports · 2025Article
- Threshold-Triggered Immune Dysregulation Precedes Clinical COPD: A Stage-Specific Diagnostic Model Combining Cytokine Profiling and Lymphocyte Phenotyping.International journal of general medicine · 2025Article
- Evaluation of selected circulating cytokines from the IL-6 family - interleukin 6, oncostatin M, and cardiotrophin-1 - in gastro-entero-pancreatic and bronchial neuroendocrine tumours.Contemporary oncology (Poznan, Poland) · 2024Article
- Peimine ameliorates LPS-induced acute lung injury by regulating Nrf2 and NF-κB pathways.American journal of translational research · 2024Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-6 (IL-6) is a cytokine synthesized by many cells in the human body. IL-6 binds to a membrane-bound receptor (IL-6R), which is only present on hepatocytes, some epithelial cells, and some leukocytes. The complex of IL-6 and IL-6R binds to the ubiquitously expressed receptor subunit gp130, which forms a homodimer and thereby initiates intracellular signaling, e.g., the JAK/STAT and MAPK pathways. Proteases can cleave the membrane-bound IL-6R from the cell surface and generate a soluble IL-6R (sIL-6R), which retains its ability to bind IL-6. The IL-6/sIL-6R complex associates with gp130 and induces signaling even on cells which do not express the IL-6R. This paradigm has been called IL-6 trans-signaling, whereas signaling via the membrane-bound IL-6R is referred to as classic signaling. We have generated several molecular tools to differentiate between both pathways and to analyze the consequences of cellular IL-6 signaling in vivo. One of these tools is soluble gp130Fc, which selectively inhibits IL-6 trans-signaling. This protein under the WHO name Olamkicept has successfully undergone phase II clinical trials in patients with autoimmune diseases. Here, in this chapter, we describe several molecular tools to differentiate between IL-6 classic and trans-signaling and to analyze the consequences of cellular IL-6 signaling in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.