IL6R Gene

Last updated on: 27.03.2022

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Definition
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The IL6R gene (IL6R stands for "interleukin 6 receptor") is a protein-coding gene located on chromosome 1q21.3. The IL6R gene encodes a subunit of the interleukin 6 (IL6) receptor complex. Alternatively spliced transcript variants encoding different isoforms have been identified in this gene. A pseudogene of this gene is located on chromosome 9.

General information
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Interaction of interleukin 6 with the membrane-bound IL6R/ IL6ST receptor complex stimulates "classical signaling," with localized expression of IL6R restricting classical IL6 signaling to a few tissues such as the liver and some cells of the immune system.

Signaling via membrane-bound IL6R is mainly regenerative and anti-inflammatory. Transformants Drives naive CD4(+) T cells into the Th17 lineage by"cluster signaling" through dendritic cells.

The soluble form of the IL6 receptor(sIL6R) acts as an agonist of IL6 activity. The IL6/sIL6R complex (hyper-IL6) binds to IL6ST/gp130 on cell surfaces and induces signaling even to cells that do not express membrane-bound IL6R. This process is referred to as IL6 'trans-signaling'. The soluble IL6 receptor (sIL6R) is causative for the proinflammatory properties of IL6. It continues to be a key player in the development of chronic inflammatory diseases. In complex with IL6, it is required for the induction of VEGF production and plays a protective role in liver injury. 'Trans-signaling' in the central nervous system regulates energy and glucose homeostasis.

Note(s)
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The receptor subunit encoded by IL6R binds only with low affinity to IL6, but does not transmit a signal via this binding. Signal activation requires association with the "interleukin 6 signal transducer" IL6ST.

Complexation leads to regulation of the immune response, acute phase responses, and hematopoiesis.

Dysregulated production of IL6 and its receptor is associated with the development of many diseases:

Literature
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  1. Spencer S et al (2019) Loss of the interleukin-6 receptor causes immunodeficiency, atopy, and abnormal inflammatory responses. J Exp Med 216: 1986-1998.

Outgoing links (3)

Cd4; Hyper-IgE-Syndrome 5; Vegf;

Last updated on: 27.03.2022