The DOI matches its Crossref record; 116 of the 116 references it cites were found in a registry or an index.
The IL-6/sIL-6R complex as a novel target for therapeutic approaches
Abstract
IL-6 plays a pivotal role in immune responses and certain oncologic conditions. The intense investigation of its biological activity and function led to the discovery of two different IL-6-driven signalling pathways. Binding to the membrane-bound IL-6 receptor (mIL-6R, CD126) causes the recruitment of two gp130 co-receptor molecules (CD130) and the activation of intracellular signalling cascades via gp130. Although this classical pathway is mainly limited to hepatocytes, neutrophils, monocytes/macrophages and certain other leukocyte populations, which express IL-6R on their surface, an alternative mechanism has also been described. Proteolytic cleavage of the mIL-6R protein or translation from alternatively spliced mRNA leads to the generation of a soluble form of the IL-6R (sIL-6R), which is likewise able to bind to IL-6. The resulting IL-6/sIL-6R complex is also capable of binding to gp130 and inducing intracellular signalling. Through this so-called 'trans-signalling' mechanism, IL-6 is able to stimulate cells that lack an endogenous mIL-6R. High levels of IL-6 and sIL-6R have been reported in several chronic inflammatory and autoimmune diseases as well as in cancer. Preclinical animal disease models have provided strong evidence that specific blockade of IL-6-regulated signalling pathways represents a promising approach for the therapy of these diseases. An optimised variant of the recently described fusion protein sgp30Fc is now heading towards its clinical evaluation.
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Citations
Cites
Interleukin-6-type cytokine signalling through the gp130/Jak/STAT pathway
HEINRICH, P. C., BEHRMANN, I., MÜLLER-NEWEN, G., SCHAPER, F., & GRAEVE, L. (1998) · Biochemical Journal · doi:10.1042/bj3340297 · Cited by 2,130
Toll Pathway-Dependent Blockade of CD4 + CD25 + T Cell-Mediated Suppression by Dendritic Cells
Pasare, C., & Medzhitov, R. (2003) · Science · doi:10.1126/science.1078231 · Cited by 1,997
Manolagas, S. C., & Jilka, R. L. (1995) · New England Journal of Medicine · doi:10.1056/nejm199502023320506 · Cited by 1,668
Gauldie, J., Richards, C., Harnish, D., Lansdorp, P., & Baumann, H. (1987) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.84.20.7251 · Cited by 1,635
Xing, Z., Gauldie, J., Cox, G., Baumann, H., Jordana, M., Lei, X. F., & Achong, M. K. (1998) · Journal of Clinical Investigation · doi:10.1172/jci1368 · Cited by 1,498
gp 130 AND THE INTERLEUKIN-6 FAMILY OF CYTOKINES
Taga, T., & Kishimoto, T. (1997) · Annual Review of Immunology · doi:10.1146/annurev.immunol.15.1.797 · Cited by 1,461
Increased Osteoclast Development After Estrogen Loss: Mediation by Interleukin-6
Jilka, R. L., Hangoc, G., Girasole, G., Passeri, G., Williams, D. C., Abrams, J. S., Boyce, B., Broxmeyer, H., & Manolagas, S. C. (1992) · Science · doi:10.1126/science.1621100 · Cited by 1,442
Interleukin-6 triggers the association of its receptor with a possible signal transducer, gp130
Taga, T., Hibi, M., Hirata, Y., Yamasaki, K., Yasukawa, K., Matsuda, T., Hirano, T., & Kishimoto, T. (1989) · Cell · doi:10.1016/0092-8674(89)90438-8 · Cited by 1,396
Interleukin-6 in Biology and Medicine
Akira, S., Taga, T., & Kishimoto, T. (1993) · Advances in Immunology · doi:10.1016/s0065-2776(08)60532-5 · Cited by 1,389
Atreya, R., Mudter, J., Finotto, S., Müllberg, J., Jostock, T., Wirtz, S., Schütz, M., Bartsch, B., Holtmann, M., Becker, C., et al. (2000) · Nature Medicine · doi:10.1038/75068 · Cited by 1,293
Self-citation
Cited by
The pro- and anti-inflammatory properties of the cytokine interleukin-6
Scheller, J., Chalaris, A., Schmidt-Arras, D., & Rose-John, S. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2011.01.034 · Cited by 3,212
Self-citationMuscle as an Endocrine Organ: Focus on Muscle-Derived Interleukin-6
Pedersen, B. K., & Febbraio, M. A. (2008) · Physiological Reviews · doi:10.1152/physrev.90100.2007 · Cited by 2,388
Rose-John, S. (2012) · International Journal of Biological Sciences · doi:10.7150/ijbs.4989 · Cited by 1,040
“These experiments allowed to decide whether the gp130 driven disease model was based on IL-6 classic signaling or IL-6 trans-signaling [54, 55].”
BackgroundMethodSelf-citationThe role of JAK/STAT signaling pathway and its inhibitors in diseases.
Xin, P., Xu, X., Deng, C., Liu, S., Wang, Y., Zhou, X., Ma, H., Wei, D., & Sun, S. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2020.106210 · Cited by 1,010
Jones, G., Sebba, A., Gu, J., Lowenstein, M. B., Calvo, A., Gomez-Reino, J. J., Siri, D. A., Tomšič, M., Alecock, E., Woodworth, T., et al. (2010) · Annals of the Rheumatic Diseases · doi:10.1136/ard.2008.105197 · Cited by 797
Metadata
- Authors
- Rose-John, S., Waetzig, G. H., Scheller, J., Grötzinger, J., & Seegert, D.
- Venue
- Expert Opinion on Therapeutic Targets
- Publisher
- Informa UK Limited
- Published
- 2007-04-27
- Volume
- 11
- Issue
- 5
- Pages
- 613-624
- ISSN
- 1472-8222 (ISSN-L)
- 1744-7631
- OpenAlex
- W2018498519
- Cited by
- 360
- References
- 116
- FWCI
- 12.68
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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