Journal
INFLAMMATION
Volume 36, Issue 3, Pages 582-591Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-012-9580-0
Keywords
asthma; Tim-3; CD4+T cell; siRNA
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Funding
- Natural Science Foundation of Hubei Province [320.6750.1285, 2010CDB08804]
- Foundation of Wuhan Health Bureau [WX11B10]
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Since CD4+ T cells play a pivotal role in the development of airway inflammation and hyperresponsiveness, targeting activated CD4+ T cell subsets and increasing the cells with regulatory function would be a logical therapeutic approach. We showed that this outcome can be achieved by local therapy with Tim-3, which is a negative regulator of CD4+ T cells. Tim-3 expression was up-regulated by ovalbumin (OVA) induction. Attenuating Tim-3 expression by RNA interference suppressed allergen-induced immune responses. Intranasal application of Tim-3 shRNA diminished airway inflammation and hyperresponsiveness. Multiple mechanisms were involved in the inhibitory effects, including regulation the imbalance of Th1/Th17 and increasing Treg cell expression. Our results indicate that the Tim-3 pathway is highly involved in the regulation of asthma. Targeting Tim-3 by siRNA may hold therapeutic potential in preventing the development of allergic asthma.
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