2016
DOI: 10.1016/j.jaci.2015.05.004
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RhoA orchestrates glycolysis for T H 2 cell differentiation and allergic airway inflammation

Abstract: Background Mitochondrial metabolism is known to be important for T cell activation. However, its involvement in effector T cell differentiation has just begun to gain attention. Importantly, how metabolic pathways are integrated with T cell activation and effector cell differentiation and function remains largely unknown. Objective We sought to test our hypothesis that RhoA GTPase orchestrates glycolysis for Th2 cell differentiation and Th2-mediated allergic airway inflammation. Methods Conditional RhoA-de… Show more

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Cited by 77 publications
(105 citation statements)
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“…In this aspect, mammalian target of rapamycin (mTOR)‐regulated glycolysis has been shown to be essential for Th17 differentiation . As we have shown that RhoA promotes mTOR signaling in activated T cells and RhoA promotes Th2 differentiation through glycolysis, it will be interesting to determine whether mTOR‐regulated glycolysis contributes to RhoA‐mediated Th17 differentiation in future. In addition, RhoA functions through activation of its immediate downstream effectors such as Rho‐associated protein kinase (ROCK), mDia, and protein kinase N .…”
Section: Discussionmentioning
confidence: 99%
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“…In this aspect, mammalian target of rapamycin (mTOR)‐regulated glycolysis has been shown to be essential for Th17 differentiation . As we have shown that RhoA promotes mTOR signaling in activated T cells and RhoA promotes Th2 differentiation through glycolysis, it will be interesting to determine whether mTOR‐regulated glycolysis contributes to RhoA‐mediated Th17 differentiation in future. In addition, RhoA functions through activation of its immediate downstream effectors such as Rho‐associated protein kinase (ROCK), mDia, and protein kinase N .…”
Section: Discussionmentioning
confidence: 99%
“…The floxed allele contains loxP sites flanking exon 3 of the RhoA allele. To delete RhoA in vivo in T cells, RhoA flox/flox mice were mated with mice expressing Cre recombinase under the control of a CD2 proximal promoter (Jackson Laboratory, Bar Harbor, ME) . In each experiment, age‐ (8‐ to 10‐week old) and sex‐matched RhoA flox/flox CD2 Cre+ mice (hereafter, referred to as RhoA −/− or RhoA‐deficient mice) and their WT littermates (RhoA flox/flox CD2 Cre− , referred to as WT mice) were used.…”
Section: Methodsmentioning
confidence: 99%
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“…To further verify this hypothesis, an EAE mouse model of multiple sclerosis was constructed as previously described23, BVDU was given orally once daily from day 3 post immunization until day 24, whereas the control mice were administrated with 0.9% saline. The data showed that in control group, the clinical symptoms initiated on day 13, and gradually increased until the end of the experiment, and in BVDU treatment group, disease initiated at later stage of the day 16, and more interestingly, the disease severity was also significantly alleviated (Fig.…”
Section: Resultsmentioning
confidence: 99%
“…Rho‐ROCK signaling appears to function in both the sensitization phase and effector phase of Th2‐dependent allergic inflammation. T cell‐specific deletion of RhoA impaired Th2 differentiation but not Th1 differentiation in vitro and prevented OVA‐induced allergic inflammation in vivo with reduction in IgE level, cell infiltration in the airway and Th2 cytokine production . Administration of fasudil all through the experimental period mimicked these effects of RhoA deficiency.…”
Section: Rho Signaling Research In Current Statusmentioning
confidence: 92%