Journal
CELL REPORTS
Volume 25, Issue 8, Pages 2148-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.10.074
Keywords
-
Categories
Funding
- NIH [R01 AR042527, R01 HL117913, R01 AI108906, P01 HL129941, R01 AI108891, R01 AG045779, U19 AI057266, R01 AI129191, I01 BX001669]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL129941, R01HL117913] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI129191, R01AI108891, U19AI057266, R01AI108906] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR042527] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG045779] Funding Source: NIH RePORTER
- Veterans Affairs [I01BX001669] Funding Source: NIH RePORTER
- VA [5I01BX001669-02, 5I01BX001669-04] Funding Source: Federal RePORTER
Ask authors/readers for more resources
Induction of protective vaccine responses, governed by the successful generation of antigen-specific antibodies and long-lived memory T cells, is increasingly impaired with age. Regulation of the T cell proteome by a dynamic network of microRNAs is crucial to T cell responses. Here, we show that activation-induced upregulation of miR-21 biases the transcriptome of differentiating T cells away from memory T cells and toward inflammatory effector T cells. Such a transcriptome bias is also characteristic of T cell responses in older individuals who have increased miR-21 expression and is reversed by antagonizing miR-21. miR-21 targets negative feedback circuits in several signaling pathways. The concerted, sustained activity of these signaling pathways in miR-21(high) T cells disfavors the induction of transcription factor networks involved in memory cell differentiation. Our data suggest that curbing miR-21 upregulation or activity in older individuals may improve their ability to mount effective vaccine responses.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available