期刊
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
卷 47, 期 8, 页码 597-603出版社
OXFORD UNIV PRESS
DOI: 10.1093/abbs/gmv058
关键词
IL-37b; dendritic cells; cytokines
资金
- National Basic Research Program of China [2013CB966904, 2015CB964402]
- National Natural Science Foundation of China [81273217, 81322007, 81401295]
- Tianjin Research Program of Application Foundation and Advanced Technology [12JCYBJC32800]
- Specialized Research Fund for the Doctoral Program of Higher Education of China [20121106120037]
- Technology Foundation for Selected Overseas Chinese Scholar
- Recruitment Program of Global Youth Experts
Interleukin 37b (IL-37b) plays a key role in suppressing immune responses, partially by modulating the function of dendritic cells (DCs). However, the precise mechanisms are still largely unknown. Here, we investigated the effects of IL-37b on DC maturation and T cell responses induced by DCs, and explored the involved signaling pathways. It was found that IL-37b down-regulated the expressions of co-stimulatory molecules CD80 and CD86 on DCs in vitro. At the same time, the expressions of pro-inflammatory cytokines, such as TNF-alpha and IL-6, were suppressed, while the expression of the T cell inhibitory cytokine TGF-beta was increased in IL-37b-treated DCs. In addition, the activation effect of DCs on T cells was impaired by IL-37b. We further revealed that extracellular single-regulated kinase (ERK), nuclear factor-kappa B (NF-kappa B), and mTOR-S6K signaling pathways were involved in the inhibition of DCs induced by IL-37b. This was confirmed by the similarly suppressive effect of chemical inhibitors against NF-kappa B, ERK, and S6K on the expressions of IL-6 and TNF-a in DCs. In conclusion, these results demonstrated that IL-37b suppressed DC maturation and immunostimulatory capacity in T cell priming by involving in ERK, NF-kappa B, and S6K-based inhibitory signaling pathways.
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