期刊
IMMUNITY
卷 41, 期 4, 页码 605-619出版社
CELL PRESS
DOI: 10.1016/j.immuni.2014.09.015
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资金
- NIH New Innovator Award [DP2GM111099-01]
- NHLBI Pathway to Independence Award [R00HL102228-05]
- American Cancer Society Research Scholar Grant
- Edward Mallinckrodt Jr. Foundation
- Pew Scholars Program
- NSF CAREER award [IOS-1253278]
- Packard Fellowship in Science and Engineering
- NIAID [K22 AI95375, AI107090]
- NIH [5T32DK007115-39, R03NS070141, R01CA166450-02]
Chronic inflammation is a contributing factor to most life-shortening human diseases. However, the molecular and cellular mechanisms that sustain chronic inflammatory responses remain poorly understood, making it difficult to treat this deleterious condition. Using a mouse model of age-dependent inflammation that results from a deficiency in miR-146a, we demonstrate that miR-155 contributed to the progressive inflammatory disease that emerged as Mir146a(-/-) mice grew older. Upon analyzing lymphocytes from inflamed versus healthy middle-aged mice, we found elevated numbers of T follicular helper (Tfh) cells, germinal center (GC) B cells, and autoantibodies, all occurring in a miR-155-dependent manner. Further, Cd4-cre Mir155(fl/fl) mice were generated and demonstrated that miR-155 functions in T cells, in addition to its established role in B cells, to promote humoral immunity in a variety of contexts. Taken together, our study discovers that miR-146a and miR-155 counterregulate Tfh cell development that drives aberrant GC reactions during chronic inflammation.
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