Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 121, Issue 1, Pages 57-69Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI44845
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Funding
- NIH [RO1 AI68085, R01 HL62348, R01 AI026322, RC1 HL069507]
- Bunning Food Allergy Project
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [20570146]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL062348, R01HL069507] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI026322, R01AI068085] Funding Source: NIH RePORTER
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Infection with influenza A virus represents a major public health threat worldwide, particularly m patients with asthma However, immunity induced by influenza A virus may have beneficial effects, particularly in young children, that might protect against the later development of asthma, as suggested by the hygiene hypothesis Herein, we show that infection of suckling mice with influenza A virus protected the mice as adults against allergen-induced airway hyperreactivity (AHR), a cardinal feature of asthma The protective effect was associated with the preferential expansion of CD4(-)CD8(-), but not CD4(+), NKT cells and required T-bet and TLR7 Adoptive transfer of this ell population into allergen-sensitized adult mice suppressed the development of allergen-induced AHR, an effect associated with expansion of the allergen-specific forkhead box p3(+) (Foxp3(+)) Treg cell population Influenza-induced protection was mimicked by treating suckling mice with a glycolipid derived from Helicobacter pylon (a bacterium associated with protection against asthma) that activated NKT cells in a CD1d restricted fashion These findings suggest what we believe to be a novel pathway that can regulate AHR, and a new therapeutic strategy (treatment with glycolipid activators of this NKT cell population) for asthma
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