Interleukin-17 receptor: Difference between revisions
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'''Interleukin-17 receptor''' ( | {{DISPLAYTITLE:Interleukin-17 receptor}} | ||
== Interleukin-17 receptor == | |||
[[File:5JVF.pdb.jpg|thumb|right|Structure of the Interleukin-17 receptor complex.]] | |||
The '''Interleukin-17 receptor''' (IL-17R) is a type of [[cytokine receptor]] that binds to the [[Interleukin-17]] (IL-17) family of cytokines. These receptors are critical components of the immune system, playing a key role in the inflammatory response and in the defense against pathogens. | |||
== Structure == | == Structure == | ||
The IL-17 receptor family consists of five members, designated as IL-17RA, IL-17RB, IL-17RC, IL-17RD, and IL-17RE. These receptors are characterized by a conserved SEFIR (similar expression to fibroblast growth factor genes and IL-17R) domain, which is essential for signal transduction. | |||
The IL- | |||
== Function == | == Function == | ||
IL-17 receptors are primarily expressed on [[epithelial cells]], [[endothelial cells]], and [[fibroblasts]]. Upon binding to their ligands, these receptors activate downstream signaling pathways, including the [[NF-kB]] and [[MAPK]] pathways, leading to the production of pro-inflammatory cytokines and chemokines. This response is crucial for recruiting [[neutrophils]] and other immune cells to sites of infection or injury. | |||
== Role in Disease == | |||
[[File:5JVF.pdb.jpg|thumb|left|Detailed view of the IL-17 receptor binding site.]] | |||
Dysregulation of IL-17 receptor signaling has been implicated in various [[autoimmune diseases]], such as [[psoriasis]], [[rheumatoid arthritis]], and [[multiple sclerosis]]. Overactivation of IL-17R can lead to excessive inflammation and tissue damage, while underactivation can result in increased susceptibility to infections. | |||
== | == Therapeutic Target == | ||
Given its role in inflammatory diseases, the IL-17 receptor is a target for therapeutic intervention. Monoclonal antibodies that inhibit IL-17 or its receptor are being developed and used to treat conditions like psoriasis and ankylosing spondylitis. | |||
== Related pages == | |||
* [[Interleukin-17]] | * [[Interleukin-17]] | ||
* [[ | * [[Cytokine receptor]] | ||
* [[Autoimmune disease]] | * [[Autoimmune disease]] | ||
* [[Inflammation]] | |||
[[Category:Immunology]] | [[Category:Immunology]] | ||
[[Category: | [[Category:Receptors]] | ||
Latest revision as of 11:08, 15 February 2025
Interleukin-17 receptor[edit]
The Interleukin-17 receptor (IL-17R) is a type of cytokine receptor that binds to the Interleukin-17 (IL-17) family of cytokines. These receptors are critical components of the immune system, playing a key role in the inflammatory response and in the defense against pathogens.
Structure[edit]
The IL-17 receptor family consists of five members, designated as IL-17RA, IL-17RB, IL-17RC, IL-17RD, and IL-17RE. These receptors are characterized by a conserved SEFIR (similar expression to fibroblast growth factor genes and IL-17R) domain, which is essential for signal transduction.
Function[edit]
IL-17 receptors are primarily expressed on epithelial cells, endothelial cells, and fibroblasts. Upon binding to their ligands, these receptors activate downstream signaling pathways, including the NF-kB and MAPK pathways, leading to the production of pro-inflammatory cytokines and chemokines. This response is crucial for recruiting neutrophils and other immune cells to sites of infection or injury.
Role in Disease[edit]
Dysregulation of IL-17 receptor signaling has been implicated in various autoimmune diseases, such as psoriasis, rheumatoid arthritis, and multiple sclerosis. Overactivation of IL-17R can lead to excessive inflammation and tissue damage, while underactivation can result in increased susceptibility to infections.
Therapeutic Target[edit]
Given its role in inflammatory diseases, the IL-17 receptor is a target for therapeutic intervention. Monoclonal antibodies that inhibit IL-17 or its receptor are being developed and used to treat conditions like psoriasis and ankylosing spondylitis.
