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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive March 13, 2014

 

Scientists believe Cbl-b could be manipulated in different ways
to keep excessive inflammation in check in people with allergic asthma.
It could also be inhibited in the treatment of cancers.

Image Credit: Ohio State University.






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Potential target for treating allergic asthma

The enzyme Cbl-b is supposed to ‘throw away’ the protein Stat6 if it overstays its welcome during an immune response, suggesting it could become a target for drugs treating allergic asthma and other autoimmune disorders.

New research in mice suggests the enzyme Cbl-b helps maintain immune system function by “throwing away” the protein Stat6 which plays a vital role in controlling symptoms of allergic asthma.


Led by Ohio State University researchers, the study is the first to link Cbl-b to allergic asthma using an animal model.

It parallels a 2012 Yale study in humans, suggesting a mutation in the gene that produces Cbl-b is associated with higher risk for asthma in children.

Other studies have suggested inhibiting Cbl-b could reduce tumors and lower chances for cancer spread.


Based on this assortment of results, scientists believe Cbl-b could be manipulated depending on the disorder in question. Its activity could be elevated to keep excessive inflammation in check in people with allergic asthma, or it could be inhibited in the treatment of cancers.

“We believe we have found one of the key molecules that can modify our immune response. We feel we can use this basic knowledge to find small molecules that modify Cbl-b’s function and treat human diseases including autoimmunity, asthma and tumors,” says Jian Zhang, associate professor of microbial infection and immunity at Ohio State University, and senior author of the study.

Allergic asthma is the most common form of asthma and is triggered by inhaling allergens such as dust mites, pet dander, pollen or mold, leading to inflamed and swollen airways in the lungs, according to the American Academy of Allergy Asthma & Immunology.

Cbl-b is a key enzyme participating in a cellular process designed to keep protein levels stable during the immune response. It is the final step in the process of moving the protein Stat6 - when its job is finished - to a space in the cell acting much like a garbage can, where it is degraded. If Stat6 is active for too long, it overstimulates Th2 and, to a lesser extent, Th9 cells — which then create excessive inflammation in the lung airways. Cbl-b alone ensures Stat6 is deleted.

“Without Stat6, Th2 is not active and Th9 is dramatically reduced. So we had minimal airway inflammation — not the abnormal, excessive inflammation present if Stat6 remains active. This suggests another factor is involved in Th9 – which we have yet to isolate,” said Zhang

Next, Zhang and colleagues will investigate Cbl-b’s potential role in response to infectious diseases. Zhang also hopes to collaborate with pharmacy experts to develop small molecules capable of modifying the enzyme’s function.

Research results are available in the journal Cell Reports.

Highlights
Loss of Cbl-b results in heightened Th2/Th9 responses and severe airway inflammation
Cbl-b is the E3 ubiquitin ligase for Stat6
Stat6 deficiency abrogates hyper-Th2 responses but partially impairs Th9 responses
Cbl-b regulates Th9 in both Stat6-dependent and -independent mechanisms

Summary
E3 ubiquitin ligase Cbl-b has emerged as a gatekeeper that controls the activation threshold of the T cell antigen receptor and maintains the balance between tolerance and autoimmunity. Here, we report that the loss of Cbl-b facilitates T helper 2 (Th2) and Th9 cell differentiation in vitro. In a mouse model of asthma, the absence of Cbl-b results in severe airway inflammation and stronger Th2 and Th9 responses. Mechanistically, Cbl-b selectively associates with Stat6 upon IL-4 ligation and targets Stat6 for ubiquitination and degradation. These processes are heightened in the presence of T cell receptor (TCR)/CD28 costimulation. Furthermore, we identify K108 and K398 as Stat6 ubiquitination sites. Intriguingly, introducing Stat6 deficiency into Cblb−/− mice abrogates hyper-Th2 responses but only partially attenuates Th9 responses. Therefore, our data reveal a function for Cbl-b in the regulation of Th2 and Th9 cell differentiation.

Authors
Guilin Qiaol, Haiyan Ying, Yixia Zhao, Yanran Liang, Hui Guo, Huifeng Shen, Zhenping Li, Julian Solway, Enxiang Tao, Y. Jeffrey Chiang, Stanley Lipkowitz, Josef M. Penninger, Wallace Y. Langdon, Jian Zhangs

Contact: Jian Zhang, (614) 292-9447; Jian.Zhang@osumc.edu
Written by Emily Caldwell, (614) 292-8310; Caldwell.151@osu.edu

This work was supported by the National Institutes of Health and the American Heart Association. Zhang also has been an American Lung Association Career Investigator.

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