Pleiotropy and specificity: insights from the interleukin 6 family of cytokines
Open accessAbstract
Since the molecular cloning of interleukin-6 (IL-6) in 1986, many other cytokines have been found to share the same signal transducer, gp130, in their receptor complexes. Thus, the IL-6 family of cytokines now consists of ten members. Although some of the family members' functions are redundant as a result of the expression of gp130, there are also functional distinctions between members. The mechanisms that determine functional redundancies and distinctions are not completely understood. Yet, research has clarified the role of IL-6 family cytokines in autoimmune diseases and has led to effective therapies that target them. Here, we review the IL-6 family of cytokines in autoimmune diseases, with a particular focus on the prototypical member IL-6, from the viewpoints of their structure, signaling, and biological features and discuss possible mechanisms of their functional pleiotropy.
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Binding of IL-6 to IL-6RA and gp130 leads to activation of JAK/STAT3 and, to a lesser extent, YAP.
“Binding of IL-6 to IL-6RA and gp130 leads to activation of JAK/ STAT3 and, to a lesser extent, YAP.23”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [23]
The supplied passages and further searches for IL-6 receptor signaling, STAT3, and YAP returned only reference URLs, with no substantive text or section/page labels. Our accessible copy therefore cannot establish whether the paper supports the claimed activation of JAK/STAT3 and, to a lesser extent, YAP. (LLM, conf=0.76)
Experimental — accuracy not yet measuredProper transduction of the IL-6 signal requires IL-6 receptor IL-6RA and co-receptor gp130.
“Proper transduction of the IL-6 signal requires IL-6 receptor IL-6RA and co-receptor gp130.23”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [23]
The supplied passages and further searches for IL-6RA, gp130, and the IL-6 receptor complex returned only reference links, with no substantive text or section/page labels. Our accessible copy therefore does not establish whether the paper says both receptors are required for IL-6 signal transduction. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIL-6/STAT3 signaling is mainly involved in the proinflammatory response.
“As IL-6/STAT3 signaling is mainly involved in the proinflammatory response, 23 it was unexpected that it controlled cell identity conversion in liver injury.”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [23]
The supplied passages and searches for IL-6/STAT3 inflammation and “pro-inflammatory” returned only reference URLs, with no substantive passage or section/page text. Our available copy therefore does not establish whether the paper characterizes IL-6/STAT3 signaling as mainly proinflammatory. (LLM, conf=0.78)
Experimental — accuracy not yet measuredIL-6 is a prototypical member of the IL-6 family of cytokines, which is composed of 10 members including IL-6, IL-11, IL-27, OSM, LIF, CNTF, CT-1, CLCF1, IL-35 and IL-39.
“IL-6 is a prototypical member of the IL-6 family of cytokines, which is composed of 10 members including IL-6, IL-11, IL-27, oncostatin M (OSM), leukemia inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), cardiotrophin 1 (CT-1), cardiotrophin-like cytokine factor 1 (CLCF1), IL-35 and IL-39 (33).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [33]
The supplied passages have no section or page labels and contain only reference links, not discussion of the IL-6 family. Searches for the ten-member list, IL-39, and “prototypical member” returned no substantive passage, so our copy cannot verify the claimed membership or count. (LLM, conf=0.72)
Experimental — accuracy not yet measuredThe IL-6R is composed of an IL-6-binding receptor molecule (IL-6Rα) and a signal transducer, gp130, which is shared among the IL-6 family of cytokines.
“The IL-6R is composed of an IL-6-binding receptor molecule (IL-6Rα) and a signal transducer, gp130, which is shared among the IL-6 family of cytokines (Fig. 1A) (33).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [33]
The passages from our copy contain reference links and corrupted section headings, but no readable discussion of IL-6R composition. Searches for IL-6Rα, gp130, and shared IL-6-family receptor subunits returned no passage that addresses the claim. (LLM, conf=0.72)
Experimental — accuracy not yet measured
IL-6 transcription is induced by a variety of stimuli, such as Toll-like receptor ligands, IL-1, TNFα, reactive oxygen species and zinc, and also depends on epigenetic regulation.
“IL-6 transcription is induced by a variety of stimuli, such as Toll-like receptor (TLR) ligands, IL-1, TNFα, reactive oxygen species (ROS) and zinc (Zn) and also depends on epigenetic regulation (33, 82, 84–86).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [33]
The available copy shows a corrupted table of contents with a heading for “Regulation of IL-6 Family Cytokine Expression,” but no readable passage from that section (page unavailable). Searches for Toll-like receptor ligands, zinc, reactive oxygen species, and epigenetic regulation returned only reference links or corrupted headings, so the copy cannot verify the claimed transcriptional regulators. (LLM, conf=0.72)
Experimental — accuracy not yet measuredThe trans-signaling mode plays crucial roles in chronic inflammation.
“Indeed, this mode plays crucial roles in chronic inflammation (33, 96).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [33]
The supplied passage has no section or page label and consists of reference links, not discussion of trans-signaling. Searches of our copy for “trans-signaling,” “chronic inflammation,” and related IL-6 signaling terms found no substantive passage addressing the claim. (LLM, conf=0.72)
Experimental — accuracy not yet measuredFor IL-6 activity, expression of both IL-6Rα and gp130 on the cell surface is required, which limits target cells to lymphocytes, myeloid cells and hepatocytes.
“For IL-6 activity, the expression of both IL-6Rα and gp130 on the cell surface is required, which limits the number of target cells on which IL-6 acts to lymphocytes, myeloid cells and hepatocytes (33).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [33]
The supplied passages and searches for IL-6Rα/gp130 expression and classic IL-6 signaling returned only reference links, with no substantive text or section/page labels. Our copy therefore provides no passage establishing whether cell-surface expression of both receptors is required or whether IL-6 target cells are limited to the three named groups. (LLM, conf=0.75)
Experimental — accuracy not yet measuredADAM17 increases sIL-6Rα, which activates STAT3 through gp130 on a variety of non-immune cells including fibroblasts, endothelial cells and epithelial cells.
“Furthermore, ADAM17 increases sIL-6Rα, which activates STAT3 through gp130 on a variety of non-immune cells including fibroblasts, endothelial cells and epithelial cells (33, 96).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [33]
The supplied passages and additional searches for ADAM17, sIL-6R, gp130, STAT3, and fibroblasts returned only reference links, with no section or page text addressing the claim. Our copy therefore provides no passage by which to assess the proposed signaling mechanism or the listed cell types. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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- Authors
- Murakami, M., Kamimura, D., & Hirano, T.
- Affiliations
- Hokkaido University (JP)
- Corresponding author
- Hirano, Toshio
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2019-04
- Volume
- 50
- Issue
- 4
- Pages
- 812-831
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2936183454
- Cited by
- 533
- References
- 280
- Citations by year
- 2026: 52 · 2025: 70 · 2024: 76 · 2023: 69 · 2022: 90 · 2021: 98 · 2020: 63 · 2019: 15
- FWCI
- 6.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
- QST-Repository (National Institutes for Quantum and Radiological Science and Technology) (submittedVersion, cc-by-nc-nd)
- Funders
- JSPS-KAKENHI
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Keywords
- interleukin-6, IL-6 family cytokines, gp130, cytokine signaling, functional redundancy, pleiotropy, specificity, autoimmune disease, cytokine structure, therapeutic targeting
- MeSH terms
- Interleukin-6 Inhibitors, Animals, Autoimmune Diseases, Gene Expression Regulation, Multigene Family, Inflammation, Structure-Activity Relationship, Signal Transduction, Interleukin-6, Cytokines, Receptors, Cytokine, Receptors, Interleukin-6, Protein Subunits, Mice, Genetic Pleiotropy
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