Interleukin-10: Difference between revisions

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== '''Interlukin-10''' '''[[2H24]]''' ==
<StructureSection load='2h24' size='350' side='right' caption='' scene='Sandbox_165/Interleukin-10/1' pspeed='8'>
===Crystal structure of human IL-10===
[[Image:2h24.png|right|thumb| Figure 1. IL-10 N-Terminus of helix A ]]
This is a cytokine.<ref> Yoon SI, Logsdon NJ, Sheikh F, Donnelly RP, Walter MR, J Biol Chem. 2006 Nov 17;281(46):35088-96. Epub 2006 Sep 18. PMID:16982608</ref>  Cytokines function as....<ref>Reference 2</ref>
'''[[2h24|2H24]]''' is the PDB id assigned to Interleukin-10 (IL-10) after the determination of the crystal structure. IL-10 is a ternary complex that requires specific assembly for proper function. The IL-10 complex is composed of IL-10,IL-10R1,IL-10R2 (R=receptor). The initial step is the formation of IL-10 and IL-10R1, a binary complex that generates a conformational change. This conformational change is required for IL-10R2 to be able to associate with the binary complex and form the ternary complex <ref name="ref1">PMID:16982608</ref>
The affinity of IL-10R1 and Il-10R2 are not considered to be dependent on the amino acid sequence but something more complex. There are several homolog IL-10s and mimic IL-10s that are able to bind and signal through the IL-10 receptor complex causing overlaying signals with cIL-10 <ref name="ref1"/>. The completed ternary complex activates the [http://en.wikipedia.org/wiki/JAK-STAT_signaling_pathway JAK/STAT signaling pathway].[[Image:IL10.png|left|thumb|'''Figure 2. Sequential assembly of the ternary complex''' ]] The completion of the ternary complex is dependent on the conformational changes that occur in the N terminus of the helix labelled A. The conformational changes occur when the cIL-10 binds with IL-10R1. There is a positional change of about 1 angstrom at residues between Cys-12 and Leu-46. There are structural features that allow for the large conformational changes, the structural features are a Cys-12 to Cys-108 disulfide bond at the N terminus and Leu-Leu-Leu motifat the C terminus of the AB loop<ref name="ref1"/>.
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=='''IL-10'''==
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Interleukin-10 is in the class [http://en.wikipedia.org/wiki/Cytokine cytokine].<ref name="ref1"/>  Interleukin-10 is a very powerful anti-inflammatory cytokine that is most commonly found to be produce by moncytes <ref>PMID:15772682</ref>. IL-10 has the ability to be a immunosupressive as well as a anti-angiogenic this means that it has the ability both promot and inhibit tumors<ref>PMID:16122836</ref>.
[[Image:2h24.png|center|150px]]
There are many types of cytokines that have many funtions such as antiinflammatory cytokines,cytokine synthesis inhibitory factor and proinflammitory cytokines<ref name="ref4"> PMID:8163935</ref>.


There are many [http://en.wikipedia.org/wiki/interleukin interleukins] that fall within the cytokine class such as IL-1,IL-2,IL-3,IL-4...IL-31,IL-32,IL-33,IL-3 and IL-35. 


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[[Image:Illu_synovial_joint.jpg|left|thumb|'''Figure 3. Synovial Joint''' ]]<ref>http://en.wikipedia.org/wiki/Synovial_membrane</ref>
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<table style="background-color:#ffffc0" cellpadding="8" width="95%" border="0"><tr><td>Please do NOT make changes to this Sandbox until after April 23, 2010. Sandboxes 151-200 are reserved until then for use by the Chemistry 307 class at UNBC taught by Prof. [[User:Andrea Gorrell|Andrea Gorrell]].</td></tr>
Shelly Huebert


IL-10 has been investigated for its role in patients with [http://en.wikipedia.org/wiki/Rheumatoid_Arthritis Rheumatoid Arthritis] (RA) as well as those with [http://en.wikipedia.org/wiki/Osteoarthritis Osteoarthritis] (OA)<ref name="ref4"/>.
RA is an autoimmune disorder that affects the [http://en.wikipedia.org/wiki/Synovial_membrane synovial] tissues via chronic synovitis. Chronic synovitis often results in joint destruction due to re-absorption of bone and the distruction of cartilage<ref name="ref5"> PMID:19758192</ref> <ref name="ref4"/>.
IL-10 is found to be spontaneously produce in synovial tissue of patients with RA and OA but not in normal synovial tissue. The variation in secretion of IL-10 is thought to be 75% under the control of the genetics of the individual<ref name="ref5"/>. When IL-10 is present there is an inhibition of the proinflammatory cytokines, namely TFN-α, IL-1α, IL-1β, IL-6, IL-8 <ref>PMID:1940799</ref>.




</StructureSection>
==3D structures of interleukin==


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== '''References''' ==
== '''References''' ==
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====
[1] Ref1

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Andrea Gorrell, Shelly Huebert, David Canner, Jaime Prilusky, Michal Harel, Alexander Berchansky