NonO Is a Novel Co-factor of PRDM1 and Regulates Inflammatory Response in Monocyte Derived-Dendritic Cells
- Title
- NonO Is a Novel Co-factor of PRDM1 and Regulates Inflammatory Response in Monocyte Derived-Dendritic Cells
- Author
- 장수화
- Keywords
- PRDM1; NonO; IL-6; inflammation; dendritic cells
- Issue Date
- 2020-07
- Publisher
- FRONTIERS MEDIA SA
- Citation
- FRONTIERS IN IMMUNOLOGY, v. 11, article no. 1436
- Abstract
- Proper expression of the transcription factor, Positive regulatory domain 1 (PRDM1), is required for maintaining homeostasis of human monocyte derived-dendritic cells (MO-DCs). The molecular mechanisms and gene targets of PRDM1 in B and T lymphocytes have been identified. However, the function of PRDM1 in dendritic cells (DCs) remains unclear. We investigate co-regulators of PRDM1 in MO-DCs identified by mass spectrometry (MS) and co-immunoprecipitation (Co-IP). Notably, non-POU domain-containing octamer-binding protein (NonO) was found to be a PRDM1 binding protein in the nucleus of MO-DCs. NonO is recruited to the PRDM1 binding site in the promoter region of IL-6. Knockdown of NonO expression by siRNA lessened suppression of IL-6 promoter activity by PRMD1 following LPS stimulation. While NonO binding to PRDM1 was observed in human myeloma cell lines, an effect of NonO on IL-6 expression was not observed. Thus, loss of NonO interrupted the inhibitory effect of PRDM1 on IL-6 expression in MO-DCs, but not plasma cells. Moreover, MO-DCs with low expression of PRDM1 or NonO induce an increased number of IL-21-producing T-FH-like cellsin vitro. These data suggest that low level of PRDM1 and NonO lead to enhanced activation of MO-DCs and the regulation of MO-DC function by PRDM1 is mediated through cell lineage-specific mechanisms.
- URI
- https://www.frontiersin.org/articles/10.3389/fimmu.2020.01436/fullhttps://repository.hanyang.ac.kr/handle/20.500.11754/169393
- ISSN
- 1664-3224
- DOI
- 10.3389/fimmu.2020.01436
- Appears in Collections:
- RESEARCH INSTITUTE[S](부설연구소) > ETC
- Files in This Item:
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