Abstract：
:NOD2 is an intracellular sensor that contributes to immune defense and inflammation. Here we investigated whether NOD2 mediates its effects through control of microRNAs (miRNAs). miR-29 expression was upregulated in human dendritic cells (DCs) in response to NOD2 signals, and miR-29 regulated the expression of multiple immune mediators. In particular, miR-29 downregulated interleukin-23 (IL-23) by targeting IL-12p40 directly and IL-23p19 indirectly, likely via reduction of ATF2. DSS-induced colitis was worse in miR-29-deficient mice and was associated with elevated IL-23 and T helper 17 signature cytokines in the intestinal mucosa. Crohn's disease (CD) patient DCs expressing NOD2 polymorphisms failed to induce miR-29 upon pattern recognition receptor stimulation and showed enhanced release of IL-12p40 on exposure to adherent invasive E. coli. Therefore, we suggest that loss of miR-29-mediated immunoregulation in CD DCs might contribute to elevated IL-23 in this disease.
journal_name
Immunityjournal_title
Immunityauthors
Brain O,Owens BM,Pichulik T,Allan P,Khatamzas E,Leslie A,Steevels T,Sharma S,Mayer A,Catuneanu AM,Morton V,Sun MY,Jewell D,Coccia M,Harrison O,Maloy K,Schönefeldt S,Bornschein S,Liston A,Simmons Adoi
10.1016/j.immuni.2013.08.035subject
Has Abstractpub_date
2013-09-19 00:00:00pages
521-36issue
3eissn
1074-7613issn
1097-4180pii
S1074-7613(13)00387-7journal_volume
39pub_type
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